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Foams are ubiquitous in human life and can be found in a variety of products and materials, such as sodas and sponges. There are liquid foams and solid foams, both of which have distinct properties useful for various applications. This book reviews, researches, and summarizes the potential uses of foam fluids and porous foams in engineering, medicine, and other industries. Chapters discuss different types of foams including multiphase foams, cellular foams, and ceramic foams as well as foam-generating mechanisms and techniques.

Foam.

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Foam. --- Colloids

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It is by now widely recognized that atherosclerosis – with its burden of consequences in cerebro- and cardiovascular diseases – is just a chronic inflammatory process of the arterial wall. A very peculiar, complex and as yet still poorly understood process, upon which hundreds of scientists from several different fields are continuously concentrating their investigative efforts in search of possible leads to therapeutic approaches. Initiation of the disease is given by deposition of lipid in the intimal layers, resulting in endothelial activation and infiltration of blood-derived mononuclear cells. These mature into macrophages, become activated, express scavenger receptors such as SR-A and CD36 and ingest the oxidized lipoprotein accumulating in the lesion. Macrophages thus represent an obvious target for intervention, as they play a crucial role in the progression of the atherosclerotic inflammation. Studies have shown that hypercholesterolaemia can increase monocyte mobilisation from bone marrow into the circulation, and several chemokines and their receptors are involved in the recruitment of blood borne monocytes into the arterial wall. Monocyte-derived macrophages are capable of sustaining their local proliferation, but resident macrophages possibly also participate in progression of the disease. Remarkably, smooth muscle cells can acquire macrophage-like features during atherogenesis, including the ability to uptake lipid, thus becoming a significant proportion of the CD68+ so called ‘foam cells’. Lipid-laden macrophages induce extracellular matrix degradation, while lipid uptake eventually causes their death with formation of a necrotic core. The efficiency in clearance of dead cells by phagocytes (efferocytosis), can also be considered as a determinant of plaque vulnerability. An important feature of macrophages is their great plasticity and functional diversity in response to signals from the plaque microenvironment. Several such ‘signals’ (cholesterol, oxidative stress, hypoxia, cytokines…) can in fact modulate cell differentiation at transcriptional and epigenetic levels, thus altering the balance between the effector vs. reparative functions of macrophages. A whole gamut of specific subsets are thus originated, which appear to be simultaneously present in lesions with proportions that vary according to their location, the disease stage, and the presence of additional cell types such as e.g. dendritic cells. The result is a multiplicity of potential pharmacological targets, representing a major obstacle for the devisement of therapeutic strategies. Experimental approaches have been attempted in diverse directions: e.g. modulating the macrophage phenotype to an anti-inflammatory and resolving state, or blocking pro-inflammatory cytokines that macrophages produce, or alternatively enhancing efferocytosis in order to favour the resolution of inflammation and stabilization of plaques. Blocking monocyte recruitment was proposed in order to hinder the initial steps of atherogenesis. Other treatments were aimed to inhibiting local proliferation of pro-inflammatory macrophages. Specific targeting of macrophages has however to date not yet provided significant, translational results. The present Research Topic collects articles to help unravel the complexity of macrophage behaviour in atherosclerosis and identify innovative pharmacological approaches.

Science: general issues --- Pharmacology --- monocytes/macrophages --- inflammation --- foam cell formation --- smooth muscle cells --- atherosclerosis progression

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It is by now widely recognized that atherosclerosis – with its burden of consequences in cerebro- and cardiovascular diseases – is just a chronic inflammatory process of the arterial wall. A very peculiar, complex and as yet still poorly understood process, upon which hundreds of scientists from several different fields are continuously concentrating their investigative efforts in search of possible leads to therapeutic approaches. Initiation of the disease is given by deposition of lipid in the intimal layers, resulting in endothelial activation and infiltration of blood-derived mononuclear cells. These mature into macrophages, become activated, express scavenger receptors such as SR-A and CD36 and ingest the oxidized lipoprotein accumulating in the lesion. Macrophages thus represent an obvious target for intervention, as they play a crucial role in the progression of the atherosclerotic inflammation. Studies have shown that hypercholesterolaemia can increase monocyte mobilisation from bone marrow into the circulation, and several chemokines and their receptors are involved in the recruitment of blood borne monocytes into the arterial wall. Monocyte-derived macrophages are capable of sustaining their local proliferation, but resident macrophages possibly also participate in progression of the disease. Remarkably, smooth muscle cells can acquire macrophage-like features during atherogenesis, including the ability to uptake lipid, thus becoming a significant proportion of the CD68+ so called ‘foam cells’. Lipid-laden macrophages induce extracellular matrix degradation, while lipid uptake eventually causes their death with formation of a necrotic core. The efficiency in clearance of dead cells by phagocytes (efferocytosis), can also be considered as a determinant of plaque vulnerability. An important feature of macrophages is their great plasticity and functional diversity in response to signals from the plaque microenvironment. Several such ‘signals’ (cholesterol, oxidative stress, hypoxia, cytokines…) can in fact modulate cell differentiation at transcriptional and epigenetic levels, thus altering the balance between the effector vs. reparative functions of macrophages. A whole gamut of specific subsets are thus originated, which appear to be simultaneously present in lesions with proportions that vary according to their location, the disease stage, and the presence of additional cell types such as e.g. dendritic cells. The result is a multiplicity of potential pharmacological targets, representing a major obstacle for the devisement of therapeutic strategies. Experimental approaches have been attempted in diverse directions: e.g. modulating the macrophage phenotype to an anti-inflammatory and resolving state, or blocking pro-inflammatory cytokines that macrophages produce, or alternatively enhancing efferocytosis in order to favour the resolution of inflammation and stabilization of plaques. Blocking monocyte recruitment was proposed in order to hinder the initial steps of atherogenesis. Other treatments were aimed to inhibiting local proliferation of pro-inflammatory macrophages. Specific targeting of macrophages has however to date not yet provided significant, translational results. The present Research Topic collects articles to help unravel the complexity of macrophage behaviour in atherosclerosis and identify innovative pharmacological approaches.

Science: general issues --- Pharmacology --- monocytes/macrophages --- inflammation --- foam cell formation --- smooth muscle cells --- atherosclerosis progression

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Global concern about climate change caused by the exploitation of fossil fuels is encouraging the use of renewable energies. For instance, the European Union aims to be climate neutral by 2050. Biogas is an interesting renewable energy source due to its high calorific value. Today, biogas is mainly used for the production of electricity and heat by a combined heat and power engine. However, before its valorization, biogas needs to be desulfurized (H2S removal) to avoid corrosion and sulfur oxides emissions during its combustion. Biogas can be upgraded (CO2 removal) and used as vehicle fuel or injected into the natural gas grid. In the last 15 years, significant advances have occurred in the development of biological desulfurization processes. In this book with five chapters, the reader can find some of the latest advances in the biogas desulfurization and an overview of the state-of-the-art research. Three of them are research studies and two are reviews concerning the current state of biogas desulfurization technologies, economic analysis of alternatives, and the microbial ecology in biofiltration units. Biogas desulfurization is considered to be essential by many stakeholders (biogas producers, suppliers of biogas upgrading devices, gas traders, researchers, etc.) all around the world.

biotrickling filters --- in-situ biogas desulphurisation --- response surface methodology --- microbial ecology --- anoxic biotrickling filter --- desulfurization --- molecular techniques --- open-pore polyurethane foam --- anaerobic digestion --- autotrophic denitrification --- anoxic biofiltration --- Teflon --- biotrickling filter --- biogas --- desulphurisation --- H2S --- post-biogas desulphurisation --- hydrogen sulfide elimination --- removal process --- Ottengraf’s model --- packing material --- hydrogen sulfide --- open polyurethane foam --- sulfur-oxidizing bacteria --- anoxic --- PVC --- biofiltration --- PET