The impact of the Fourth Industrial Revolution on the services innovation

Cel – Artykuł poświęcony jest czwartej rewolucji przemysłowej i innowacyjności usług. Przedstawiono w nim istotę Przemysłu 4.0, podjęto próbę wskazania zjawisk występujących w obszarze usług będących efektem dyfuzji nowych technologii, porównano usługi oraz produkcję w odniesieniu do innowacji. Podano także praktyczne przykłady obszarów mplementacji nowych technologii w usługach. Metoda badań – Metodą badawczą była analiza literatury z zakresu czwartej rewolucji przemysłowej, studium przypadku – formy i obszary zastosowania w praktyce oraz własna obserwacja zmian, jakie zachodzą na rynku usług w kontekście nowych technologii. Wnioski – Obecnie sektor usług i jego potencjał innowacyjny determinowany jest nowymi technologiami, które w coraz większym stopniu w sposób bezpośredni i pośredni oddziałują na oferowane usługi i procesy usługowe, implikując tym samym ciągłą ich ewolucję. Oryginalność / wartość / implikacje / rekomendacje – Zakładając, że rozwój nowych technologii 4.0 będzie postępował, powstaje konieczność intensyfikacji badań interdyscyplinarnych nad problemem innowacyjności usług w świetle szybkiego generowania nowych rozwiązań i zacierania się granicy pomiędzy produktem a usługą.Purpose – The article is devoted to the Fourth Industrial Revolution and services innovation. It presents the essence of Industry 4.0, attempts to identify phenomena occurring in the area of services resulting from the spread of new technologies, as well as compares services and production with reference to innovation. Also, some practical examples of the areas of implementation of the new technologies in services are given. Research method – The research method was the analysis of literature and a case study – forms and areas of application in practice as well as author’s own observation of the changes taking place on the service market in the context of the new technologies. Results – Currently, the service sector and its innovative potential are determined by new technologies, which increasingly, directly and indirectly affect the provided services and service processes, thus implying their constant evolution. Originality / value / implications / recommendations – Assuming that the development of new 4.0 technologies will continue, there is a need to intensify the interdisciplinary research on the problem of service innovation in the light of the rapid generation of new solutions and the blurring of the boundary between the product and the [email protected]ł Ekonomiczno-Socjologiczny, Uniwersytet ŁódzkiAyres R.U., 1986, Technological protection and piracy: some implications for policy, „Technological Forecasting and Social Change”, vol. 30(1), pp. 5-18, DOI: 10.1016/0040-1625(86)90052-1.Christensen C.M., 2010, Przełomowe innowacje – możliwości rozwoju czy zagrożenie dla przedsiębiorstwa, Wydawnictwo Naukowe PWN, Warszawa.den Hertog P., 2000, Knowledge-intensive business services as co-producers of innovation, „International Journal of Innovation Management”, vol. 4(4), pp. 491-528, DOI: 10.1142/S136391960000024X.Działalność innowacyjna przedsiębiorstw w latach 2016-2018, 2019, GUS, Warszawa–Szczecin.Kline S.J., Rosenberg N., 1986, An overview of innovation, [in:] The positive sum strategy: harnessing technology for economic growth, Landau R., Rosenberg N. (eds.), National Academy Press, Washington.Li G., Hou Y., Wu A., 2017, Fourth industrial revolution: technological drivers, impacts and coping methods, „Chinese Geographical Science”, vol. 27, pp. 626-637, DOI: 10.1007/s11769-017-0890-x.Miller M., 2016, Internet rzeczy: jak inteligentne telewizory, samochody, domy i miasta zmieniają świat, Wydawnictwo Naukowe PWN, Warszawa.Podręcznik OSLO 2018. Zalecenia dotyczące pozyskiwania, prezentowania i wykorzystywania danych z zakresu innowacji. Pomiar działalności naukowo-technicznej i innowacyjnej, 2020, GUS, Warszawa–Szczecin.Popławski K., Bajczuk R., 2019, Przemysł 4.0. Nowa polityka przemysłowa Niemiec, Ośrodek Studiów Wschodnich, Warszawa.Schumpeter J.A., 2003, Capitalism, socialism and democracy, Routledge, London–New York.Schwab K., 2016, The fourth industrial revolution, World Economic Forum, Geneva, Switzerland.Skalfist P., Mikelsten D., Teigens V., 2020, Sztuczna inteligencja: czwarta rewolucja przemysłowa, Cambridge Stanford Books, e-book.Szukalski S.M., 2018, Wybrane aspekty innowacyjności i konkurencyjności przedsiębiorstw, [w:] Innowacje i trendy we współczesnej gospodarce, Szukalski S.M., Wodnicka M., Wentura--Dudek B. (red.), FIDAS, Kraków.Ustundag A.E. Cevikcan, 2017, Industry 4.0. managing The digital transformation, Springer International Publishing, Switzerland.Wodnicka M., 2019, Technologie blockchain przyszłością logistyki, „Zeszyty Naukowe Małopolskiej Wyższej Szkoły Ekonomicznej w Tarnowie”, t. 41(1), s. 43-54, DOI: 10. 25944/znmwse.2019.01.4354.Wyszkowska-Kuna J., 2016, Usługi biznesowe oparte na wiedzy. Wpływ na konkurencyjność gospodarki na przykładzie wybranych krajów Unii Europejskiej, Wydawnictwo Uniwersytetu Łódzkiego, Łódź.www 1, https://ibs.org.pl/app/uploads/2018/06/IBS_Policy_Paper_02_2018_pl.pdf [data dostępu: 3.09.2020].www 2, http://www.wnp.pl/wiadomosci/jakub-dzik-wiceprezes-impela-pracownicy -z-zagranicy-pomaga-nam-wzrastac-gospodarczo,297301.html [data dostępu: 25.08.2020].www 3, https://www.accenture.com/_acnmedia/Accenture/next-gen-4/tech-vision -2017/pdf/Accenture-TV17-Short.pdf?la=en [data dostępu: 25.09.2020].www 4, https://ccnews.pl/2017/02/15/sztuczna-inteligencja-zmieni-caly-sektorbpo/[data dostępu: 25.08.2020].www 5, https://przemysl-40.pl/index.php/2020/01/03/5g-roboty-medyczne-i-rozszerzona-rzeczywistosc/ [data dostępu: 3.09.2020].3(105)485

Isolation and Culture of Pulmonary Endothelial Cells from Neonatal Mice

Endothelial cells provide a useful research model in many areas of vascular biology. Since its first isolation 1, human umbilical vein endothelial cells (HUVECs) have shown to be convenient, easy to obtain and culture, and thus are the most widely studied endothelial cells. However, for research focused on processes like angiogenesis, permeability or many others, microvascular endothelial cells (ECs) are a much more physiologically relevant model to study 2. Furthermore, ECs isolated from knockout mice provide a useful tool for analysis of protein function ex vivo. Several approaches to isolate and culture microvascular ECs of different origin have been reported to date 3-7, but consistent isolation and culture of pure ECs is still a major technical problem in many laboratories. Here, we provide a step-by-step protocol on a reliable and relatively simple method of isolating and culturing mouse lung endothelial cells (MLECs). In this approach, lung tissue obtained from 6- to 8-day old pups is first cut into pieces, digested with collagenase/dispase (C/D) solution and dispersed mechanically into single-cell suspension. MLECS are purified from cell suspension using positive selection with anti-PECAM-1 antibody conjugated to Dynabeads using a Magnetic Particle Concentrator (MPC). Such purified cells are cultured on gelatin-coated tissue culture (TC) dishes until they become confluent. At that point, cells are further purified using Dynabeads coupled to anti-ICAM-2 antibody. MLECs obtained with this protocol exhibit a cobblestone phenotype, as visualized by phase-contrast light microscopy, and their endothelial phenotype has been confirmed using FACS analysis with anti-VE-cadherin 8 and anti-VEGFR2 9 antibodies and immunofluorescent staining of VE-cadherin. In our hands, this two-step isolation procedure consistently and reliably yields a pure population of MLECs, which can be further cultured. This method will enable researchers to take advantage of the growing number of knockout and transgenic mice to directly correlate in vivo studies with results of in vitro experiments performed on isolated MLECs and thus help to reveal molecular mechanisms of vascular phenotypes observed in vivo

Microstructural evolution of TiO₂-doped silica gels during heating

Properties of silica glass, doped with TiO₂, obtained by the sol-gel technique were examined as depending on the heating method, using the microstructural investigation methods. It has been found that the greatest specific surface and porosity are obtained immediately after the removal of water and organic substances at the temperature of about 300 °C. With increasing heating temperature the specific surface and the porosity decrease, especially above 900 °C. The mode the pores are Hnked with each other is also changed. The pores assume the character of "through-pores", open at both ends, and their closing takes place only with the lapse of time. The heating rate does not exert any essential influence on the product properties after heating, nevertheless slow heating favours the preservation of the primary microstructure of gel

Innowacje rynku usług w redefinicji działalności usługowej

The article is described to innovation in services and innovative solutions in corporations. Models of service delivery are presented as an example of innovative solutions in organizational structures

Rho-stimulated contractility drives the formation of stress fibers and focal adhesions

Activated rhoA, a ras-related GTP-binding protein, stimulates the appearance of stress fibers, focal adhesions, and tyrosine phosphorylation in quiescent cells (Ridley, A.J., and A. Hall, 1992. Cell. 70:389-399). The pathway by which rho triggers these events has not been elucidated. Many of the agents that activate rho (e.g., vasopressin, endothelin, lysophosphatidic acid) stimulate the contractility of smooth muscle and other cells. We have investigated whether rho's induction of stress fibers, focal adhesions, and tyrosine phosphorylation is the result of its stimulation of contractility. We demonstrate that stimulation of fibroblasts with lysophosphatidic acid, which activates rho, induces myosin light chain phosphorylation. This precedes the formation of stress fibers and focal adhesions and is accompanied by increased contractility. Inhibition of contractility by several different mechanisms leads to inhibition of rho-induced stress fibers, focal adhesions, and tyrosine phosphorylation. In addition, when contractility is inhibited, integrins disperse from focal adhesions as stress fibers and focal adhesions disassemble. Conversely, upon stimulation of contractility, diffusely distributed integrins are aggregated into focal adhesions. These results suggest that activated rho stimulates contractility, driving the formation of stress fibers and focal adhesions and elevating tyrosine phosphorylation. A model is proposed to account for how contractility could promote these events

Rap1b is required for normal platelet function and hemostasis in mice

Rap1b, an abundant small GTPase in platelets, becomes rapidly activated upon stimulation with agonists. Though it has been implicated to act downstream from G protein–coupled receptors (GPCRs) and upstream of integrin αIIbβ3, the precise role of Rap1b in platelet function has been elusive. Here we report the generation of a murine rap1b knockout and show that Rap1b deficiency results in a bleeding defect due to defective platelet function. Aggregation of Rap1b-null platelets is reduced in response to stimulation with both GPCR-linked and GPCR-independent agonists. Underlying the defective Rap1b-null platelet function is decreased activation of integrin αIIbβ3 in response to stimulation with agonists and signaling downstream from the integrin αIIbβ3. In vivo, Rap1b-null mice are protected from arterial thrombosis. These data provide genetic evidence that Rap1b is involved in a common pathway of integrin activation, is required for normal hemostasis in vivo, and may be a clinically relevant antithrombotic therapy target

Small GTPase Rap1 Is Essential for Mouse Development and Formation of Functional Vasculature

BACKGROUND: Small GTPase Rap1 has been implicated in a number of basic cellular functions, including cell-cell and cell-matrix adhesion, proliferation and regulation of polarity. Evolutionarily conserved, Rap1 has been studied in model organisms: yeast, Drosophila and mice. Mouse in vivo studies implicate Rap1 in the control of multiple stem cell, leukocyte and vascular cell functions. In vitro, several Rap1 effectors and regulatory mechanisms have been proposed. In particular, Rap1 has been implicated in maintaining epithelial and endothelial cell junction integrity and linked with cerebral cavernous malformations. RATIONALE: How Rap1 signaling network controls mammalian development is not clear. As a first step in addressing this question, we present phenotypes of murine total and vascular-specific Rap1a, Rap1b and double Rap1a and Rap1b (Rap1) knockout (KO) mice. RESULTS AND CONCLUSIONS: The majority of total Rap1 KO mice die before E10.5, consistent with the critical role of Rap1 in epithelial morphogenesis. At that time point, about 50% of Tie2-double Rap1 KOs appear grossly normal and develop normal vasculature, while the remaining 50% suffer tissue degeneration and show vascular abnormalities, including hemorrhages and engorgement of perineural vessels, albeit with normal branchial arches. However, no Tie2-double Rap1 KO embryos are present at E15.5, with hemorrhages a likely cause of death. Therefore, at least one Rap1 allele is required for development prior to the formation of the vascular system; and in endothelium-for the life-supporting function of the vasculature

Tyrosine phosphorylation is involved in reorganization of the actin cytoskeleton in response to serum or LPA stimulation

Tyrosine phosphorylation is known to regulate the formation of focal adhesions in cells adhering to extracellular matrix (ECM). We have investigated the possible involvement of tyrosine phosphorylation and the focal adhesion kinase (FAK) in the cytoskeletal changes induced by serum or lysophosphatidic acid (LPA) in quiescent Swiss 3T3 fibroblasts. As shown previously by others, quiescent cells stimulated with serum or LPA reveal a rapid reappearance of focal adhesions and stress fibers. Here we show that this is accompanied by an increase in phosphotyrosine in focal adhesions and specifically an increase in the tyrosine phosphorylation of FAK. The LPA-stimulated reappearance of focal adhesions and stress fibers is blocked by inhibitors of phospholipase C but not by pertussis toxin (PTX), indicating that this LPA signaling pathway is mediated by phospholipase C activation and does not involve PTX-sensitive G proteins. In the absence of serum or LPA, these cytoskeletal effects and the tyrosine phosphorylation of FAK can be mimicked by sodium orthovanadate in conjunction with hydrogen peroxide, agents that inhibit protein tyrosine phosphatases and thereby elevate levels of phosphotyrosine. Two tyrosine kinase inhibitors, erbstatin and genistein block both the serum-induced tyrosine phosphorylation of FAK and the assembly of focal adhesions and stress fibers. Two other tyrosine kinase inhibitors, tyrphostins 47 and 25, previously shown to inhibit FAK, failed to prevent FAK phosphorylation or the reassembly of focal adhesions and stress fibers in response to serum. However, these inhibitors did prevent FAK phosphorylation and cytoskeletal assembly in response to lysophosphatidic acid (LPA), one component of serum previously shown to stimulate assembly of focal adhesions and stress fibers. Our findings suggest that the response to serum is complex and that although FAK phosphorylation is important, other tyrosine kinases may also be involved

Focal adhesions, contractility, and signaling

Focal adhesions are sites of tight adhesion to the underlying extracellular matrix developed by cells in culture. They provide a structural link between the actin cytoskeleton and the extracellular matrix and are regions of signal transduction that relate to growth control. The assembly of focal adhesions is regulated by the GTP-binding protein Rho. Rho stimulates contractility which, in cells that are tightly adherent to the substrate, generates isometric tension. In turn, this leads to the bundling of actin filaments and the aggregation of integrins (extracellular matrix receptors) in the plane of the membrane. The aggregation of integrins activates the focal adhesion kinase and leads to the assembly of a multicomponent signaling complex