59 research outputs found
Business development in renewable energy
This paper discusses how to foster development of renewable energy business. Factors that impede or enhance renewable energy in the EU 27 member states in the period 1998–2008 are analyzed. Nine factors are considered: population density, production output and energy sector output to indicate market conditions, public total expenditures, subsidies and environmental protection expenditures to indicate institutional conditions, R&D, share of students in population and venture capital to indicate firm’s resources. Scarce space for business development and vested energy interests are the main impediments. R&D and venture capital are main drivers. The US and EU support for R&D and venture capital in renewable energy are compared. The US support is larger and mainly based on R&D grants. It has generated large, innovative enterprises. The EU support is mainly based on price guarantees for renewable energy delivery to grid. It has generated many enterprises. Building capabilities through stakeholders’ networks in early phase of business development and clusters in the later phase is recommended
Homocysteine, vitamin B12 and folate levels in premature coronary artery disease
BACKGROUND: Hyperhomocysteinemia is known as an independent risk factor of atherosclerosis, but the probable role of hyperhomocysteinemia in premature Coronary Artery Disease (CAD) is not well studied. The aim of this study was to assess the role of hyperhomocysteinemia, folate and Vitamin B12 deficiency in the development of premature CAD. METHODS: We performed an analytical case-control study on 294 individuals under 45 years (225 males and 69 females) who were admitted for selective coronary angiography to two centers in Tehran. RESULTS: After considering the exclusion criteria, a total number of 225 individuals were enrolled of which 43.1% had CAD. The mean age of participants was 39.9 +/- 4.3 years (40.1 +/- 4.2 years in males and 39.4 +/- 4.8 years in females). Compared to the control group, the level of homocysteine measured in the plasma of the male participants was significantly high (14.9 +/- 1.2 versus 20.3 +/- 1.9 micromol/lit, P = 0.01). However there was no significant difference in homocysteine level of females with and without CAD (11.8 +/- 1.3 versus 11.5 ± 1.1 micromol/lit, P = 0.87). Mean plasma level of folic acid and vitamin B12 in the study group were 6.3 +/- 0.2 and 282.5 +/- 9.1 respectively. Based on these findings, 10.7% of the study group had folate deficiency while 26.6% had Vitamin B12 deficiency. Logistic regression analysis for evaluating independent CAD risk factors showed hyperhomocysteinemia as an independent risk factor for premature CAD in males (OR = 2.54 0.95% CI 1.23 to 5.22, P = 0.01). Study for the underlying causes of hyperhomocysteinemia showed that male gender and Vitamin B12 deficiency had significant influence on incidence of hyperhomocysteinemia. CONCLUSION: We may conclude that hyperhomocysteinemia is an independent risk factor for CAD in young patients (bellow 45 years old) – especially in men -and vitamin B12 deficiency is a preventable cause of hyperhomocysteinemia
NADPH oxidases in cardiovascular disease: insights from in vivo models and clinical studies
NADPH oxidase family enzymes (or NOXs) are the major sources of reactive oxygen species (ROS) that are implicated in the pathophysiology of many cardiovascular diseases. These enzymes appear to be especially important in the modulation of redox-sensitive signalling pathways that underlie key cellular functions such as growth, differentiation, migration and proliferation. Seven distinct members of the family have been identified of which four (namely NOX1, 2, 4 and 5) may have cardiovascular functions. In this article, we review our current understanding of the roles of NOX enzymes in several common cardiovascular disease states, with a focus on data from genetic studies and clinical data where available
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
Dual-specificity phosphatase 1 ubiquitination in extracellular signal-regulated kinase-mediated control of growth in human hepatocellular carcinoma.
Sustained activation of extracellular signal-regulated kinase
(ERK) has been detected previously in numerous tumors in the
absence of RAS-activating mutations. However, the molecular
mechanisms responsible for ERK-unrestrained activity independent
of RAS mutations remain unknown. Here, we evaluated
the effects of the functional interactions of ERK proteins
with dual-specificity phosphatase 1 (DUSP1), a specific inhibitor
of ERK, and S-phase kinase-associated protein 2 (SKP2)/
CDC28 protein kinase 1b (CKS1) ubiquitin ligase complex in
human hepatocellular carcinoma (HCC). Levels of DUSP1, as
assessed by real-time reverse transcription–PCR and Western
blot analysis, were significantly higher in tumors with better
prognosis (as defined by the length of patients’ survival) when
compared with both normal and nontumorous surrounding
livers, whereas DUSP1 protein expression sharply declined
in all HCC with poorer prognosis. In the latter HCC subtype,
DUSP1 inactivation was due to either ERK/SKP2/CKS1-
dependent ubiquitination or promoter hypermethylation
associated with loss of heterozygosity at the DUSP1 locus.
Noticeably, expression levels of DUSP1 inversely correlated
with those of activated ERK, as well as with proliferation index
and microvessel density, and directly with apoptosis and
survival rate. Subsequent functional studies revealed that
DUSP1 reactivation led to suppression of ERK, CKS1, and
SKP2 activity, inhibition of proliferation and induction of
apoptosis in human hepatoma cell lines. Taken together, the
present data indicate that ERK achieves unrestrained activity
during HCC progression by triggering ubiquitin-mediated
proteolysis of its specific inhibitor DUSP1. Thus, DUSP1 may
represent a valuable prognostic marker and ERK, CKS1, or
SKP2 potential therapeutic targets for human HC
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