The protection of domain names through trademarks

The protection of domain names through trademarks The main purpose of my thesis is to define a status of domain names from a legal standpoint and also to analyze the possibility of covering the protection of domain names through trademarks. Assuming that a domain name fulfills conditions stipulated by a law it may become a subject to trademark laws and can be registered as a trademark in the register kept by the Industrial Property Office. The thesis is composed of five chapters. The first part of introductory chapter focuses on the technical aspects of domain names and institutions directly related to domain names. It focuses on history of the Internet, IP addresses and DNS servers. The second part of the first chapter is devoted to the structure and registration of domain names and also to foreign institutions directly related to of the Internet and its domain names. The second chapter describes the status of domain names in the Czech legal system and compares the legislation of Act no. 40/1964 Coll., The Civil Code and Act no. 89/2012 Coll., The Civil Code, relating to domain names as the subject of civil relations. The main subject of the third chapter are trademarks. This chapter defines the concept, function and types of trademarks. Furthermore, this chapter describes absolute and relative..

The Molecular Mechanisms of Iron Metabolism and Its Role in Cardiac Dysfunction and Cardioprotection

Iron is an essential mineral participating in different functions of the organism under physiological conditions. Numerous biological processes, such as oxygen and lipid metabolism, protein production, cellular respiration, and DNA synthesis, require the presence of iron, and mitochondria play an important role in the processes of iron metabolism. In addition to its physiological role, iron may be also involved in the adaptive processes of myocardial “conditioning”. On the other hand, disorders of iron metabolism are involved in the pathological mechanisms of the most common human diseases and include a wide range of them, such as type 2 diabetes, obesity, and non-alcoholic fatty liver disease, and accelerate the development of atherosclerosis. Furthermore, iron also exerts potentially deleterious effects that may be manifested under conditions of ischemia/reperfusion (I/R) injury, myocardial infarction, heart failure, coronary artery angioplasty, or heart transplantation, due to its involvement in reactive oxygen species (ROS) production. Moreover, iron has been recently described to participate in the mechanisms of iron-dependent cell death defined as “ferroptosis”. Ferroptosis is a form of regulated cell death that is distinct from apoptosis, necroptosis, and other types of cell death. Ferroptosis has been shown to be associated with I/R injury and several other cardiac diseases as a significant form of cell death in cardiomyocytes. In this review, we will discuss the role of iron in cardiovascular diseases, especially in myocardial I/R injury, and protective mechanisms stimulated by different forms of “conditioning” with a special emphasis on the novel targets for cardioprotection

Diastolic dysfunction in prediabetic male rats: role of mitochondrial oxidative stress

Although incidence and prevalence of prediabetes are increasing, little is known on its cardiac effects. Therefore, our aim was to investigate the effect of prediabetes on cardiac function and to characterize parameters and pathways associated with deteriorated cardiac performance. Long-Evans rats were fed with either control or high-fat chow for 21 weeks and treated with a single low dose (20 mg/kg) streptozotocin at week 4. High-fat and streptozotocin treatment induced prediabetes as characterized by slightly elevated fasting blood glucose, impaired glucose- and insulin tolerance, increased visceral adipose tissue and plasma leptin levels, as well as sensory neuropathy. In prediabetic animals a mild diastolic dysfunction was observed, the number of myocardial lipid droplets increased, and left ventricular mass and wall thickness were elevated, however, no molecular sign of fibrosis or cardiac hypertrophy was evidenced. In prediabetes, production of reactive oxygen species was elevated in subsarcolemmal mitochondria. Expression of mitofusin-2 was increased while the phosphorylation of phospholamban and expression of Bcl-2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3, a marker of mitophagy) decreased. However, expression of other markers of cardiac auto- and mitophagy, mitochondrial dynamics, inflammation, heat shock proteins, Ca2+/calmodulin-dependent protein kinase II, mTOR or apoptotic pathways were unchanged in prediabetes. This is the first comprehensive analysis of cardiac effects of prediabetes indicating that mild diastolic dysfunction and cardiac hypertrophy are multifactorial phenomena which is associated with early changes in mitophagy, cardiac lipid accumulation and elevated oxidative stress, and that prediabetes-induced oxidative stress originates from the subsarcolemmal mitochondria