Books on the topic 'Lipid Probes'

The rise in the incidence of infections is caused by multi drug resistant (MDR) bacteria, it is essential to elucidate the basic mechanism of antibiotic resistance to discover effective methods for diagnosis and treatment of infections. The use of pathogen-specific probes offers a faster alternative for pathogen detection and could improve the diagnosis of infection. High resolution melting analysis techniques are useful for the detection of multi drug resistant pathogens. Rational Structural Based Drug Design is a common method to identify a lead compound and take it forward for further developments. This book provides information about recent strategies involved in the diagnosis and treatment of infections caused by MDR bacteria. The volume covers the use of molecular probes for the quantification of pathogenic bacteria, along with other techniques mentioned above. Chapters also cover the use of identification of novel drug targets from the Lipid A biosynthesis and also from quorum sensing mediated biofilm formation in MDR bacteria. Chapters also cover herbal alternatives for the treatment of MDR bacteria like the use of Cassia aungustifolia in treatment of various diseases. The reference is suitable for biomedical students, cellular and molecular biologists.

Inflammation results from a complex interaction between a large number of mediators able to induce each other and to favour the generation of other inflammatory molecules (e.g. free radicals, lipid mediators, and proteases). The perpetuation of inflammation by these cascades of mediators is favoured by their ability to induce coagulation, leukocyte recruitment, and cell and tissue alteration (apoptosis, necrosis, and barrier disruption). Other cascades of mediators occur to generate anti-inflammatory mediators favouring the healing process. A neuroendocrine loop and neuromediators from central and peripheral nervous system are also involved in the process, allowing a return to homeostasis.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

This article examines the applications of nanoparticles in medicine. Nanomedicine is a promising field that can make available different nanosystems whose novel, usually size-dependent, physical, chemical and/or biological properties are exploited to combat the disease of interest. One kind of particulate systems represents a vast array of either metallic,semiconductor, polymeric, protein or lipid nanoparticles that can be exploited for diagnosis and treatment of various diseases. This article first provides an overview of general issues related to physicochemical and biological properties of different nanoparticles. It then considers the current problems associated with the use of nanoparticles in medicine and suggests some solutions. It also discusses the interaction of nanoparticles with cells and factors that determine these interactions and concludes with some examples of new approaches for real-time imaging of experimental animals that could be useful, complementary methods for evaluations of effectiveness (or toxicity) of novel nanomaterials andnanomedicines.

Metabolism is driven by redox reactions, in which part of the difference in potential energy between the electron donor and acceptor is used by the organism for its life processes (with the remainder being dissipated as heat). The key process is intermediary metabolism, by which the energy stored in reserves (glycogen, starch, lipid, protein) is transferred to ATP. In aerobic respiration the electrons released from reserves are passed to oxygen, which is thereby reduced to water. Not all ATP regeneration involves oxygen as the final electron acceptor, and not all oxygen is used for ATP regeneration, but oxygen consumption is often the simplest and most practical way to measure the rate of intermediary metabolism and the errors in doing so are believed to be small. The costs of existence, as estimated by resting metabolism, represent only a part (~ 25%) of the daily energy expenditure of organisms. The costs of the organism’s ecology (growth, reproduction, movement and so on) are additional to existence costs. Resting metabolic rate increases with cell temperature, indicating that it costs more energy to maintain a warm cell than it does a cool or cold cell. The temperature sensitivity of resting metabolism is highly conserved across organisms.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.