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OPEN ACCESS PLUS
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Contents
Pp. 35 - 45
Graham Wilfred Ewing
[Open Access Plus] |
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The purpose of this article is to compare and evaluate the advantages and benefits of the cognitive screening technique Virtual Scanning with contemporary diagnostic and screening techniques, in particular genetic screening and biomarkers. In the last 50 years biomarker techniques and more recently genetic screening have been developed to characterise the onset, progression and regression of pathologies. Nevertheless the scientific picture is not yet complete. It does not yet include an understanding of relationship between genotype and phenotype; the regulatory function of the autonomic nervous system; or the rate or level of the expressed protein, protein conformation, the rate at which proteins react, and the reaction conditions such as pH, levels of minerals and cofactors, and temperature. By contrast, Virtual Scanning is based upon the light absorbing and emitting properties of proteins and how this bioluminescence influences colour perception. It provides a measure of the level of expressed protein and the rate at which such expressed protein subsequently reacts with its reactive substrate. The article highlights the limitations of genetic screening and biomarkers and the perceived advantages which Virtual Scanning may have for routine mass screening e.g. of diabetes, cardiovascular disease, cancers, depression, migraine, etc.
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Pp. 279 - 288
Marc J. George, Rajesh Kharbanda and Raymond J. MacAllister
[Open Access Plus] |
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Atherosclerosis is the major cause of morbidity and mortality worldwide. Endothelial dysfunction is central to the pathogenesis of atherosclerosis, initiating a triad of lipid accumulation in the vessel wall, a co-existent inflammatory response and proliferation of smooth muscle cells. It has also been implicated in the precipitation of acute ischaemia, and the determination of the extent of injury following such complications. Healthy endothelium regulates numerous blood vessel functions, including vascular tone, cell adhesiveness, and coagulation through the production of mediators. The best characterised of these are the vasodilators, nitric oxide (NO), prostacyclin, and endothelium derived hyperpolarising factor, and the vasoconstrictors thromboxane and endothelin. The endothelium itself may also be maintained by bone-marrow derived endothelial progenitor cells (EPC) which are mobilised in response to vascular injury and have angiogenic and proliferative properties. Understanding of the biology of the endothelium in atherosclerosis has led to new treatments and more may follow. Work is ongoing into NO bioavailability, prostacyclin agonists, endothelin and thromboxane antagonists, novel antiinflammatory and anti-oxidative agents as well as means of harnessing the properties of EPCs. It is hoped that this research will yield clinically useful approaches that will retard the progression of atherosclerosis and reduce the incidence or consequences of acute complications.
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Pp. 118 - 121
Mariko Kyutoku, Hironori Nakagami, Futoshi Nakagami, Hiroshi Koriyama, Mariana Kiomy Osako, Munehisa Shimamura, Takashi Miyake and Ryuichi Morishita
[Open Access Plus] |
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Lipoprotein(a) [Lp(a)] is known as an independent risk factor for cardiovascular diseases (CVD). Lp(a) is a unique lipoprotein consisting of the glycoprotein apolipoprotein(a) [apo(a)] covalently linked to apolipoproteinB-100 (apoB) in low-density lipoprotein (LDL) by a single disulfide bond. Although Lp(a) level is hugely variable and under strict genetic control, largely by apo(a) gene with kringle-4 type2 repeats, elevated level of plasma Lp(a) is correlated with CVD. Smaller isoforms with fewer kringle-4 repeats are associated with higher plasma Lp(a) level, leading to an increased risk for CVD. Lipid lowering agents (i.e. statins) have little or no effect on plasma Lp(a) level. Although it was reported that administration of niacin or estrogen may reduce the Lp(a) levels, there are no specific agents for the reduction of plasma Lp(a). In this review, we put together recent evidence and describe the overview of Lp(a) with the future direction.
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Pp. 183 - 194
Se-Jin Lee
[Open Access Plus] |
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Myostatin (MSTN) is a transforming growth factor-β family member that plays a critical role in regulating skeletal muscle mass. Genetic studies in multiple species have demonstrated that mutations in the Mstn gene lead to dramatic and widespread increases in muscle mass as a result of a combination of increased fiber numbers and increased fiber sizes. MSTN inhibitors have also been shown to cause significant increases in muscle growth when administered to adult mice. As a result, there has been an extensive effort to understand the mechanisms underlying MSTN regulation and activity with the goal of developing the most effective strategies for targeting this signaling pathway for clinical applications. Here, I review the current state of knowledge regarding the regulation of MSTN extracellularly by binding proteins and discuss the implications of these findings both with respect to the fundamental physiological role that MSTN plays in regulating tissue homeostasis and with respect to the development of therapeutic agents to combat muscle loss.
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