Clinical Medicine

New PDF release: Cardiovascular Plaque Rupture (Fundamental and Clinical

By David Brown

ISBN-10: 0203908910

ISBN-13: 9780203908914

ISBN-10: 082470276X

ISBN-13: 9780824702762

Illustrating the improvement and determinants of attainable plaque rupture, Cardiovascular Plaque Rupture offers an in-depth evaluation of the pathology, etiology, mobile and molecular biology, prognosis, and therapy of plaque within the cardiovascular system-exploring the jobs of actual pressure, irritation, and infectious brokers at the development of heart problems. represent and determine susceptible plaque utilizing novel imaging modalities and variations of present invasive and noninvasive applied sciences! Containing fresh information on preventive gene treatment and antibiotic stabilization of plaque, >Cardiovascular Plaque Rupture considers ·serine proteinase and metalloproteinase inhibitors within the prevention of plaque rupture ·lipid decreasing to stabilize plaque ·clinical trial designs to illustrate healing prevention of plaque rupture ·and extra! Discussing present tools of plaque overview, together with intravascular ultrasound and elastography, in vivo spectroscopic research, optical coherence tomography, thermography, and magnetic resonance imaging, Cardiovascular Plaque Rupture is an vital consultant for cardiologists, vascular and cardiac surgeons, radiologists, vascular biologists, endocrinologists, and fellows, citizens, and scientific institution scholars in those disciplines.

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Extra info for Cardiovascular Plaque Rupture (Fundamental and Clinical Cardiology, 45)

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In a rat model of vascular injury by balloon angioplasty, the resulting intimal hyperplasia could be blocked through the use of a specific inhibitor of PDGF-receptor tyrosine kinase (CGP53716) (187). This study indicated that PDGF-R activation was important in both SMC migration and proliferation; however, migration was shown to be affected to a greater extent. The various sources of PDGF in a plaque include endothelial cells, SMC, and platelets (188). On endothelial disruption or dysfunction, platelets can adhere to the basement membrane, resulting in release of PDGF-BB, or the endothelium can produce the PDGF-BB, which can then act as a chemotactic agent for SMC.

In the case of αthrombin, which is associated within the matrix of the media, its activation depends on both its release from the matrix on injury and the up-regulation of its receptor by bFGF (202). In addition, the expression of its receptor is associated with SMC that produce PDGF (202). Use of inhibitors of thrombin such as hirudin has been reported to reduce restenosis after angioplasty (203, 204). Although IGF-1 can increase the ability of PDGF to induce SMC proliferation, it may play a more important role in remodeling the extracellular matrix by enhancing production of hydroxyproline and increasing the organization and maturation of collagen (205).

The differential expression of C-C chemokines by different cell types in atherosclerosis suggests that chemokines may help cre- CCR5 CCR1, CCR3, CCR5 CCR4 MCP-4 MCP-5 MIP-1α MIP-1β RANTES TARC (TECK) DC, EC F, M, T EC, P, T M, M, SMC F, M, T F, M Inflammatory Inflammatory Inflammatory mitogens Inflammatory Inflammatory mitogens Inflammatory stimuli stimuli stimuli, stimuli stimuli stimuli, IFN-γ, IL-1, TNF, growth factors, LPS, mitogens, IFN, IL-1, LPS, mitogens, virus IFN, mitogens, LPS IL-1, LPS, TNF IL-1, LPS, TNF IL-1, LPS, TNF, mitogens microorganisms IFN, LPS, TNF IFN—γ Platelet activation Platelet activation Stimuli M, NK, T T N F M, T M, NK, T M, NK, T Bas, D, Eos, M, N, NK, T Bas, Eos, M N, SMC, T M, N, NK, T Bas, D, Eos, M, NK, T N, SMC, T EC, EC, EC, EC, EC, N EC, F, N, SMC B, EC, N, NK, SMC, T Target cells Eos, eosinophils; M, monocytes/macrophages; N, neutrophils; P, platelets; mT, memory T cells; ESL-1, E-selectin ligand-1; GAGs, glycosaminoglycans; PSGL-1, P-selectin glycoprotein ligand-1; SFLs, sialylated fucosylated lactosamines; EC, endothelial cells; B, B cells; Bas, basophils; D, dendratic cells, F, fibroblasts; NK, natural killer cells; SMC, smooth muscle cells; T, T cells; IFN, interferon; IL-1, interleukin-1; LPS, lipopolysaccharide; TNF, tumor necrosis factor-α CCR1, CCR2, CCR3, CCR10 CCR2, CCR3 CCR2 CCR1, CCR3, CCR5 MCP-3 F, M All types CCR2, CCR10 CCR1, CCR2, CCR5 EC, F, M, T M EC, F, SMC P EC, F, SMC EC, F, M, T EC, F, M, N, SMC, T Cells able to produce the chemokine CXCR3 CXCR3 CXCR2, (CXCR1) Unknown CXCR1, CXCR2 CXCR2, (CXCR1) CXCR1, CXCR2 MCP-2 IP-10 MIG NAP-2 PF4 CC MCP-1 CXC ENA-78 GRO (α,β,γ) IL-8 Receptor Chemokines That May Be Involved in Atherosclerosis (145, 147) Chemokine Table 2 16 Berman et al.

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Cardiovascular Plaque Rupture (Fundamental and Clinical Cardiology, 45) by David Brown

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