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90.10. MedBed and its Effect on Cultivated Intestinal Epithelial Cells and Functional Neutrophils
Abstract
Background: Quantum entanglement is a phenomenon in theoretical physics that happens when pairs or groups of particles are generated in such a way that the quantum state of each particle cannot be described independently of the others even when the particles are separated by a large distance. Material and methods: The 90.10. MedBed is a virtual bed that is quantum entangled with a 90.10.-CUBE by a quantum processor, the 9010MedBedOS. The 90.10.-CUBE was located in Akumal Quintana Roo, Mexico, 8,603 kilometers air-line distance from the cell culture laboratory conducting the tests. The 90.10. MedBed is a virtual bed that is quantum entangled with a 90.10.-CUBE by a quantum processor, the 9010MedBedOS. By the process of 90.10. quantum entanglement, the 90.10. CUBE’s basic potential is transferred to the 90.10. MedBed. For the present in vitro-study with intestinal epithelial cells and functional neutrophils – at laboratory conditions instead of a bed – seeded cells in the culture dishes were quantum entangled with the 90.10. MedBed, i.e. the system was installed on the dishes and activated in the laboratory to conduct the study. Control dishes were not treated and were incubated in the same incubator with a distance of at least 30 to 40 cm to the treated dishes. Results: For intestinal epithelial cells, a better regeneration process was determined demonstrating that 90.10. MedBed was able to promote healing processes of the intestinal cell layer and, thus, to promote intestinal and systemic health and wellbeing. The second experimental series with functional neutrophils as inflammationmediating cells demonstrated a marked decrease in the generation of reactive superoxide anion radicals by exposure to 90.10. MedBed quantum entanglement. In vivo, this influence might have a positive impact on the healing process of complicated secondary wounds or on (chronic) inflammatory processes directly. Conclusions: The results clearly demonstrate the effectiveness of the 90.10. MedBed which was quantum entangled with a 90.10.-CUBE by a quantum processor, the 9010MedBedOS, on the cellular level. The results confirm and complement previous findings on the effect of 90.10. quantum entanglement on cultured organ-specific cells in which we demonstrated an increased regeneration of cultured connective tissue fibroblasts.
... 10. Med Bed have demonstrated beneficial cellular effects [12,13]. The 90.10. ...
Neutrophils are main players in the effector phase of the host defense against micro-organisms and have a major role in the innate immune response. Neutrophils show phenotypic heterogeneity and functional flexibility, which highlight their importance in regulation of immune function. However, neutrophils can play a dual role and besides their antimicrobial function, deregulation of neutrophils and their hyperactivity can lead to tissue damage in severe inflammation or trauma. Neutrophils also have an important role in the modulation of the immune system in response to severe injury and trauma. In this review we will provide an overview of the current understanding of neutrophil subpopulations and their function during and post-infection and discuss the possible mechanisms of immune modulation by neutrophils in severe inflammation.
Neutrophils are one of the most important effector cells of the innate immune response(1). They are traditionally seen as a homogenous population of short lived cells mainly involved in the defense against extracellular micro‐organisms by phagocytosis and intracellular killing(1,2). The cells contain a large armamentarium that aids in this function and ranges from the production of reactive oxygen species by a membrane‐bound NADPH oxidase to cytotoxic proteins and peptides residing in the different granules present in the cytoplasm(3).
Recently the view of neutrophils belonging to a homogenous population of cells has been challenged and several neutrophil phenotypes have been described that exhibit specialized functions such as involvement in tissue repair, tumor killing and immune regulation(4). It is not clear whether these cells belong to separate parallel lineages originating from the bone marrow or that neutrophils become instructed in the distant tissues changing their phenotypes. In addition, functional heterogeneity in a phenotypically homogenous population of neutrophils adds to the complexity of neutrophil phenotypes(5).
This article will review the current literature describing the heterogeneity within the neutrophil compartment with respect to both phenotype and function in health and disease.
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Despite considerable recent progress in defining neutrophil functions and behaviors in tissue repair, much remains to be determined with regards to its overall role in the tissue integration of biomaterials. This article provides an overview of the neutrophil’s numerous, important roles in both inflammation and resolution, and subsequently, their role in biomaterial integration. Neutrophils function in three primary capacities: generation of oxidative bursts, release of granules and formation of neutrophil extracellular traps (NETs); these combined functions enable neutrophil involvement in inflammation, macrophage recruitment, M2 macrophage differentiation, resolution of inflammation, angiogenesis, tumor formation and immune system activation. Neutrophils exhibit great flexibility to adjust to the prevalent microenvironmental conditions in the tissue; thus, the biomaterial composition and fabrication will potentially influence neutrophil behavior following confrontation. This review serves to highlight the neutrophil’s plasticity, reiterating that neutrophils are not just simple suicidal killers, but the true maestros of resolution and regeneration.
Reactive oxygen species (ROS) are generated as by-products of normal cellular metabolic activities. Superoxide dismutase, glutathione peroxidase, and catalase are the enzymes involved in protecting cells from the damaging effects of ROS. ROS are produced in response to ultraviolet radiation, cigarette smoking, alcohol, nonsteroidal anti-inflammatory drugs, ischemia-reperfusion injury, chronic infections, and inflammatory disorders. Disruption of normal cellular homeostasis by redox signaling may result in cardiovascular, neurodegenerative diseases and cancer. ROS are produced within the gastrointestinal (GI) tract, but their roles in pathophysiology and disease pathogenesis have not been well studied. Despite the protective barrier provided by the mucosa, ingested materials and microbial pathogens can induce oxidative injury and GI inflammatory responses involving the epithelium and immune/inflammatory cells. The pathogenesis of various GI diseases including peptic ulcers, gastrointestinal cancers, and inflammatory bowel disease is in part due to oxidative stress. Unraveling the signaling events initiated at the cellular level by oxidative free radicals as well as the physiological responses to such stress is important to better understand disease pathogenesis and to develop new therapies to manage a variety of conditions for which current therapies are not always sufficient.
Scientists who study neutrophils often have backgrounds in cell biology, biochemistry, haematology, rheumatology or infectious disease. Paradoxically, immunologists seem to have a harder time incorporating these host-defence cells into the framework of their discipline. The recent literature discussed here indicates that it is appropriate for immunologists to take as much interest in neutrophils as in their lymphohaematopoietic cousins with smooth nuclei. Neutrophils inform and shape immune responses, contribute to the repair of tissue as well as its breakdown, use killing mechanisms that enrich our concepts of specificity, and offer exciting opportunities for the treatment of neoplastic, autoinflammatory and autoimmune disorders.
To the Editor: In the excellent article by Weiss on tissue destruction by neutrophils (Feb. 9 issue),¹ there is an implicit assumption that neutrophils lack endogenous reducing substances that could quench intracellular or extracellular oxidants. We would therefore like to emphasize that ascorbic acid is present in human neutrophils, in concentrations 20 to 30 times higher than in plasma.² Although the function of ascorbic acid in neutrophils is unknown, it has been proposed that it quenches free radicals,³ either within or perhaps outside neutrophils. However, before this or other functions of neutrophil ascorbic acid can be addressed, it is of…
An extremely important feature of the intestinal epithelium is its function as a physical barrier between the environment and our bodies' internal milieu. At the same time it has to allow for uptake of important nutrients. At least four different transport mechanisms exist that allow selective uptake and transport of macromolecules across the epithelial cell layer, i.e. paracellular transport, passive diffusion of molecules from the apical to the basolateral side, vesicle-mediated transcytosis and carrier-mediated uptake and diffusion through the epithelial cell layer. Each of these transport mechanisms depends on the physicochemical properties of the compound, its ability to interact with the plasma membrane, its molecular weight and size, stability and charge distribution. In vivo, parameters not directly associated with the molecule in question will influence uptake and transepithelial transport. Intestinal motility, interactions with other molecules from the diet and the digestive process like bile salts and enzymes, and solubility in the mucus layer will affect the absorption process. Thus, in vitro models for studying absorption through the intestinal epithelium have several limitations. Still, they are considered useful model systems for such purposes. Similarly, effects of bioactive molecules on the epithelium can be studied by measuring barrier function and effects on transport processes.
IPEC-J2 cells are intestinal porcine enterocytes isolated from the jejunum of a neonatal unsuckled piglet. The IPEC-J2 cell line is unique as it is derived from the small intestine and is neither transformed nor tumorigenic in nature. IPEC-J2 cells mimic the human physiology more closely than any other cell line of non-human origin. Therefore, it is an ideal tool to study epithelial transport, interactions with enteric bacteria, effects of probiotic microorganisms and the effect of nutrients and other feedstuffs on a variety of widely used parameters (e.g. transepithelial electrical resistance (TEER), permeability, metabolic activity) reflecting epithelial functionality.
IPEC-J2 cells undergo in culture a process of spontaneous differentiation that leads to the formation of a polarized monolayer with low or high TEER, depending on the type of serum added to the culture medium, within 1–2 weeks. Porcine serum gives rise to low resistance and normal active transport rates, enabling comparison with the in vivo situation. The high resistance caused by fetal bovine serum can be beneficial to use when investigating compounds having a negative effect on the monolayer permeability or tight junction structures.
There are still many opportunities for exploring the use of these cells as the available research is limited. This chapter will cover the origin, characteristics and methods of the use of IPEC-J2 cells as an in vitro model for several research applications, as well as comparisons between IPEC-J2 cells and other epithelial cell lines.
Recent advances in quantum information theory reveal the deep connections between entanglement and thermodynamics, many-body theory, quantum computing and its link to macroscopicity.
In vitro studies on the pathogenesis in swine have been hampered by the lack of relevant porcine cell lines. Since many bacterial infections are swine-specific, studies on pathogenic mechanisms require appropriate cell lines of porcine origin. We have characterized the permanent porcine intestinal epithelial cell line, IPEC-J2, using a variety of methods in order to assess the usefulness of this cell line as an in vitro infection model. Electron microscopic analyses and histochemical staining revealed the cells to be enterocyte-like with microvilli, tight junctions and glycocalyx-bound mucin. The functional integrity of monolayers was determined by transepithelial electrical resistance (TEER) measurements. Both commensal bacteria and important bacterial pathogens were chosen for study based on their principally different infection mechanisms: obligate extracellular Escherichia coli, facultative intracellular Salmonella and obligate intracellular Chlamydia. We determined the colonization and proliferation of the bacteria on and within the host cells and monitored the host cell response. We verified the expression of mRNAs encoding the cytokines IL-1alpha, -6, -7, -8, -18, TNF-alpha and GM-CSF, but not TGF-beta or MCP-1. IL-8 protein expression was enhanced by Salmonella invasion. We conclude that the IPEC-J2 cell line provides a relevant in vitro model system for porcine intestinal pathogen-host cell interactions.
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