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Telecommunication sector faces to parallel investments into both fixed and mobile (5G) networks, however return on investments lag behind profit expectations. Co-investment, like mobile network sharing is a cost efficiency enabler that may accelerate price decrease, may allow earlier, higher coverage and may improve capacity and quality parameters, like download speed, therefore altogether contributes to social welfare increase. The purpose of this paper to assess the Hungarian mobile network sharing that not cleared by the competition regulator, however has been placed in unchanged form for 8 years. The research question is to assess what is the connection between mobile network sharing and social welfare improvement at 4G - 5G mobile broadband rollout. The finding is that, majority of network sharing procompetitive effects allowing benefits, but anticompetitive effects not causing marked distortion. Affordable connectivity prices for information society roots in operators’ cost efficiency, however further research required to assess proper level of efficiency gains pass through to customers and appropriate level of access pricing to shared infrastructure for other rival operators in Hungary. Mobile Network Sharing’s benefits may outweigh potential drawbacks, but due to lack of regulatory clearance, 5G rollout launched without sharing, causing social welfare loss. The originality of the empirical research is despite network sharing not cleared, procompetitive advantages may outweigh anticompetitive ones.

A távközlési szektor párhuzamos befektetési kihívással szembesül a szélessávú vezetékes optikai és mobil 5G hálózatok kiépítésénél, ugyanakkor ezek megtérülése a normál profit elvárás alatt marad. A társberuházás, mint a mobil hálózatmegosztás költséghatékony megoldást jelent, de szabályozói aggodalmakat vet fel verseny és innováció szempontjából. A kutatási kérdés azt vizsgálta, hogy melyek a mobil hálózatmegosztás releváns pénzügyi és szabályozói értékelési szempontjai Európában, amelyek alapján ajánlást fogalmaz meg az 5G időszakra mind a szolgáltatók, mind a szabályzók számára a társdalmi jólét növekedésének elősegítésére. A kutatási módszertan kvalitatív megközelítést alkalmaz a főbb gazdasági elemzések és szabályozások áttekintésére. A hipotézis szerint a hálózatmegosztás a sűrűn lakott városi területeken sem csökkenti a versenyt és az innovációt, ezért nem káros a társadalmi jólétre. A fő következtetés és újdonságtartalom, hogy a versenyélénkítési hasznok meghaladhatják a versenykorlátozó hatásokat, így a nettó pozitív hatás hozzájárulhat a társadalmi jólét növekedéséhez.

The organism-wide effects of viral infection SARS-CoV-2 are well studied, but little is known about the dynamics of how the infection spreads in time among or within cells due to the scarcity of suitable high-resolution experimental systems. Two-photon (2P) imaging combined with a proper subcellular staining technique has been an effective tool for studying mechanisms at such resolutions and organelle levels. Herein, we report the development of a novel calcium sensor molecule along with a 2P-technique for identifying imaging patterns associated with cellular correlates of infection damage within the cells. The method works as a cell viability assay and also provides valuable information on how the calcium level and intracellular distribution are perturbed by the virus. Moreover, it allows the quantitative analysis of infection dynamics. This novel approach facilitates the study of the infection progression and the quantification of the effects caused by viral variants and viral load.

The EU digital decade 2030 connectivity targets require parallel fixed Fiber and mobile 5G investments from Mobile Network Operators, however majority of data traffic generated and monetized by Big Techs (Hyperscalers), therefore operators require a fair share contribution. The aim of this paper to compare fair share contribution to virtual and cloud technology enabled cost efficient co-investment scenario between Operators and Big Techs in RAN and Core networks. The Research Question seeks to address the question of to what extant Operators and Big Techs public cloud co-investment meet the fair share financial contribution principle for 5G rollout. The Hypothesis tested is the fair share contribution principle requested by operators and already politicians to accelerate 5G deployment. The Research Methodology employed focusing on conclusive researches mainly with descriptive analysis based on secondary data. Qualitative analysis covers incumbent and rival MNOs’ financial incentives and conduct, as well as quantitative analysis applied on consultancies forecasted financial impact. The expected finding emerged from this study is the co-investment partnership with Big Techs into public cloud provides cost efficiency to Mobile Network Operators that is already a market driven first contribution to fair cost sharing of 5G investments. The originality of the paper to call attention for this connection, so fair share contribution has a prelude that parallel is widespread.

The biology of the failing cardiomyocyte is a complex interaction of a number of abnormal pathophysiological processes involving signalling pathways, intracellular ionic fluxes, intercellular communications, oxidative stress, impaired mitochondrial energetics, altered structural morphology, abnormal reactivation of foetal gene expression patterns, and activation of cell death pathways. The crosstalk between these pathways is complex, and positive feedback between the different systems leads to the vicious cycle of deterioration of mechanical function and cell survival that characterizes the phenotype of the failing cardiomyocyte. Identifying and targeting critical nodal points and master regulatory systems may identify novel therapeutic strategies that can recover multiple elements of the failing phenotype and translate into meaningful clinical benefits for patients with heart failure.

This review aims to summarise new approaches in SARS-CoV-2-related research in cardiology. We provide a head-to-head comparison of models, such as animal research and human pluripotent stem cells, to investigate the pathomechanisms of COVID-19 and find an efficient therapy. In vivo methods were useful for studying systemic processes of the disease; however, due to differences in animal and human biology, the clinical translation of the results remains a complex task. In vitro stem cell research makes cellular events more observable and effective for finding new drugs and therapies for COVID-19, including the use of stem cells. Furthermore, multicellular 3D organoids even make it possible to observe the effects of drugs to treat SARS-CoV-2 infection in human organ models.

Cardiovascular diseases are one of the leading causes of mortality in the western world. Myocardial infarction is among the most prevalent and results in significant cell loss within the myocardium. Similarly, numerous drugs have been identified as having cardiotoxic side effects. The adult human heart is however unable to instigate an effective repair mechanism and regenerate the myocardium in response to such damage. This is in large part due to the withdrawal of cardiomyocytes (CMs) from the cell cycle. Thus, identifying, screening, and developing agents that could enhance the proliferative capacity of CMs holds great potential in cardiac regeneration. Human induced pluripotent stem cells (hiPSCs) and their cardiovascular derivatives are excellent tools in the search for such agents. This chapter outlines state-of-the art techniques for the two-dimensional differentiation and attainment of hiPSC-derived CMs and endothelial cells (ECs). Bioreactor systems and three-dimensional spheroids derived from hiPSC-cardiovascular derivatives are explored as platforms for drug discovery before focusing on relevant assays that can be employed to assess cell proliferation and viability.

Human-induced pluripotent stem cells (hiPSCs) and their differentiated derivatives became a new, promising source for in vitro screening techniques. Cell lines derived from healthy individuals can be applied for drug safety testing, while patient-derived cells provide a platform to model diseases in vitro and can be used as a tool for personalized medicine including specific drug efficacy testing and identification of new pharmacological targets as well as for tailoring pharmacological therapies. Efficient differentiation protocols yielding cardiomyocytes or endothelial cells derived from iPSCs have been developed recently. Phenotypic characterization and gene expression profiling of these derivatives can reveal clues for developmental and pathological questions. Moreover, functional analysis and cell-based assays using automated fluorescence imaging platform and high content analysis characterize cell type-specific profiles of hiPSC-derived cardiomyocytes (hiPSC-CM) and endothelial cells (hiPSC-EC) at the cellular and subcellular levels. This can be utilized in a platform which can provide multiple endpoint profiles of candidate compounds.

Human pluripotent stem cells (hPSC) are investigated as a source of authentic human cardiac cells for drug discovery and toxicological tests. Cell-based assays using automated fluorescence imaging platform and high-content analysis characterize hypertrophic and toxicity profiles of compounds in hPSC-derived cardiomyocytes (hPSC-CM) at the cellular and subcellular levels. In purified population of hPSC-CM loaded with cell tracer probe and cell death markers, both hypertrophic and toxicity profiles can be assessed in live cardiomyocyte cultures. Alternatively, in non-purified cultures of hPSC-CM, hypertrophy, proliferation, and cell death assays can be performed specifically in the cardiomyocyte subpopulation using antibodies directed against cardiac proteins and a combination of cell death- and proliferation-specific fluorescent probes.

Despite current drug therapies, cardiovascular disease remains the major cause of morbidity and mortality, which suggests that yet unknown transmitter systems might be also involved in this disease.Recent years discoveries have mainly focused on the most common type of cardiac receptors--the seven-transmembrane-spanning G-protein coupled receptors. mRNA encoding several recently discovered, orphan' receptors and their putative ligands has been identified in human tissues such as heart, vessels and plasma.Data obtained from in vitro pharmacological studies using healthy and pathological surgical samples of human arteries, veins and heart muscle as well as from subsequent in vivo studies are proving advantageous in characterization of potent vasoactive and direct cardiac effects of these peptide ligands, such as apelin, relaxin, ghrelin, and urotensin II. These novel peptides also have a clinical relevance as they are shown to be differentially expressed in human heart failure.The pharmacological characterization of these emerging peptide-receptor systems is therefore a tantalizing area of cardiovascular research, with the prospect of identifying new diagnostic and therapeutic targets.