The emerging securities market in Russia

Author's OriginalThis paper examines the Russian equity market from speculative infancy to its modern-day status as an asset in the global economy.Khambata, D. & Aybar, C. (1998). The Emerging Securities Market in Russia. Journal of East-West Business, 4(3), 5-17. doi: 10.1300/J097v04n03_0

Patterns of corporate ownership and privatization in Visegrad countries : 1989-1996

Author's OriginalThe article analyzes merger and acquisition activities in Visegrad Countries (the Czech Republic, Poland, Hungary and Slovakia). The analysis established linkages among the FDI, Privatization and M&A activities and reports the characteristics of transactions in the region in a comparative spirit. The findings indicate that majority of activities in the region involved foreign investors from Western Europe and USA. The M&A activities were concentrated in manufacturing segments such as automobiles, food processing, glass and clay, service segments such as telecom, utilities and financial services. The study also revealed some pre and post transaction ownership patterns in respective countries as well as methods of acquisition.Aybar, C., Khambata, D. & Milman, C. (2000). Patterns of Corporate Ownership and Privatization in Visegrad Countries: 1989-1996. Journal of East-West Business, 6(1), 57-80. doi:10.1300/J097v06n01_0

Investigation of the vasoprotective role of C-type natriuretic peptide

Background: Ischaemic cardiovascular disease, including myocardial infarction and stroke, is the leading cause of morbidity and mortality worldwide. Atherosclerosis and coronary artery disease, which underpin ischaemic cardiovascular disorders, are characterised by chronic inflammation of the blood vessel wall and endothelial dysfunction. C-type natriuretic peptide (CNP) has recently been identified as an endothelium-derived hyperpolarising factor with anti-atherogenic properties. The studies described herein investigated the hypothesis that the vasoprotective profile of CNP includes opposing effects on endothelial and vascular smooth muscle cell proliferation and regulation of blood pressure. Methods: Cellular incorporation of bromodeoxyuridine was used to determine cell proliferation and immunoblotting was employed to assess expression/activity of intracellular signalling proteins in human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (RAoSMC). An endothelium specific CNP knockout (ecCNP KO) mouse model was developed and organ bath pharmacology utilised to assess vascular reactivity in vitro, and radiotelemetric monitoring used to determine blood pressure in vivo. Principal findings: CNP augmented HUVEC proliferation in a natriuretic peptide receptor (NPR)-Cdependent fashion by up-regulating the cell cycle promoter, cyclin D1. In contrast, CNP increased expression of the cell cycle inhibitors p21waf1/cip1/p27kip1 in RAoSMC and reduced cell growth; the pro- and anti-mitogenic effects of CNP were mediated in an extracellular signal-regulated kinase (ERK) 1/2-dependent manner. Vascular reactivity and endothelial function were disrupted in isolated aortae from female ecCNP KO mice compared to WT, whilst in males was unchanged. Female ecCNP KO mice were hypertensive. Conclusions: The anti-atherogenic properties of CNP are mediated in part by NPR-C and ERK 1/2 signalling, resulting in a differential regulation of cell cycle proteins that promotes endothelial cell proliferation and inhibits smooth muscle cell growth. Moreover, endothelium-derived CNP is key to blood pressure regulation in females. These data suggest that targeting CNP/NPR-C signalling may represent a novel approach for the treatment of cardiovascular disease

Natriuretic peptide receptor-3 underpins the disparate regulation of endothelial and vascular smooth muscle cell proliferation by C-type natriuretic peptide

CM Panayiotou was the recipient of a Wellcome Trust Prize PhD studentship. RS Khambata was the recipient of a Medical Research Council PhD studentshi

The Noncanonical Pathway for In Vivo Nitric Oxide Generation: The Nitrate-Nitrite-Nitric Oxide Pathway.

In contrast to nitric oxide, which has well established and important roles in the regulation of blood flow and thrombosis, neurotransmission, the normal functioning of the genitourinary system, and the inflammation response and host defense, its oxidized metabolites nitrite and nitrate have, until recently, been considered to be relatively inactive. However, this view has been radically revised over the past decade and more. Much evidence has now accumulated demonstrating that nitrite serves as a storage form of nitric oxide, releasing nitric oxide preferentially under acidic and/or hypoxic conditions but also occurring under physiologic conditions: a phenomenon that is catalyzed by a number of distinct mammalian nitrite reductases. Importantly, preclinical studies demonstrate that reduction of nitrite to nitric oxide results in a number of beneficial effects, including vasodilatation of blood vessels and lowering of blood pressure, as well as cytoprotective effects that limit the extent of damage caused by an ischemia/reperfusion insult, with this latter issue having been translated more recently to the clinical setting. In addition, research has demonstrated that the other main metabolite of the oxidation of nitric oxide (i.e., nitrate) can also be sequentially reduced through processing in vivo to nitrite and then nitrite to nitric oxide to exert a range of beneficial effects-most notably lowering of blood pressure, a phenomenon that has also been confirmed recently to be an effective method for blood pressure lowering in patients with hypertension. This review will provide a detailed description of the pathways involved in the bioactivation of both nitrate and nitrite in vivo, their functional effects in preclinical models, and their mechanisms of action, as well as a discussion of translational exploration of this pathway in diverse disease states characterized by deficiencies in bioavailable nitric oxide. SIGNIFICANCE STATEMENT: The past 15 years has seen a major revision in our understanding of the pathways for nitric oxide synthesis in the body with the discovery of the noncanonical pathway for nitric oxide generation known as the nitrate-nitrite-nitric oxide pathway. This review describes the molecular components of this pathway, its role in physiology, potential therapeutics of targeting this pathway, and their impact in experimental models, as well as the clinical translation (past and future) and potential side effects

Natural mutations of human XDH promote the nitrite (NO2 −)-reductase capacity of xanthine oxidoreductase: A novel mechanism to promote redox health?

Several rare genetic variations of human XDH have been shown to alter xanthine oxidoreductase (XOR) activity leading to impaired purine catabolism. However, XOR is a multi-functional enzyme that depending upon the environmental conditions also expresses oxidase activity leading to both O2·- and H2O2 and nitrite (NO2−) reductase activity leading to nitric oxide (·NO). Since these products express important, and often diametrically opposite, biological activity, consideration of the impact of XOR mutations in the context of each aspect of the biochemical activity of the enzyme is needed to determine the potential full impact of these variants. Herein, we show that known naturally occurring hXDH mutations do not have a uniform impact upon the biochemical activity of the enzyme in terms of uric acid (UA), reactive oxygen species (ROS) and nitric oxide ·NO formation. We show that the His1221Arg mutant, in the presence of xanthine, increases UA, O2·- and NO generation compared to the WT, whilst the Ile703Val increases UA and ·NO formation, but not O2·-. We speculate that this change in the balance of activity of the enzyme is likely to endow those carrying these mutations with a harmful or protective influence over health that may explain the current equipoise underlying the perceived importance of XDH mutations. We also show that, in presence of inorganic NO2−, XOR-driven O2·- production is substantially reduced. We suggest that targeting enzyme activity to enhance the NO2−-reductase profile in those carrying such mutations may provide novel therapeutic options, particularly in cardiovascular disease

Erratum: Antiplatelet effects of dietary nitrate in healthy volunteers: Involvement of cGMP and influence of sex (Free Radical Biology and Medicine (2013) 65 (1521-1532))

A correction to an error in the original published fi

Endothelial C-type natriuretic peptide maintains vascular homeostasis

PMCID: PMC4151218Wellcome Trust (084449/Z/07/Z and 078496/Z/05/Z