Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 5

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  CARDIOVASCULAR DISEASE
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1

Cardiovascular disease - the challenge for biotechnology

100%
Pietrucha T., Szemraj J.
Biotechnologia
|
1999
|
issue 1
34-44
EN
The significance of thromboembolic complications in the etiology and development of cardiovascular diseases, such as ischaemic heart disease or myocardial infarction, is undisputable and well documented. It is commonly believed that intravascular thrombi may cause vessel narrowing and even lead to complete vessel occulsion. When encountering circulation, narrowing of vascular lumen, such as intravascular clots and platelet aggregates, is believed to result in thromboembolisms. Activation of the fibrinolytic system allows for the proteolysis of fibrin clots, the main components of vascular thrombi, and thus it may lead to vascular reperfusion. According to numerous data presented during the 15th Congress of the International Society on Thrombosis and Haemostasis (1995), the superior indications for the use of thrombolytic therapy are acute myocardial infarction and extensive pulmonary embolism. It is still more frequently used in the therapy of deep venous thrombosis and occlusions of peripheral arterial vessels. Treatment of cerebral stroke with thrombolytic agents is under experimental studies. The development of modern techniques in molecular biology, genetic engineering and biotechnology has led to the 'eruption' of quite new perspectives in thrombolytic pharmacology.
2

Current trends in biotechnology of drugs applied in cardiovascular diseases - recombinant proteins, peptide analogues and antisense oligonucleotides

100%
Cierniewski C., Stasiak M.
Biotechnologia
|
1996
|
issue 3
11-22
EN
This lecture consist of three parts, the first one gives a summary of mechanisms regulatting hemostasis and fibrynolysis, the second - discusses potential target molecules for therapeutic intervention, and the third one describes recent studies on selective inhibition of certain pathophysiological processes by molecules designed to prevent cardiovascular problems.Thus, a critical review of current trends in biotechnology of drugs which recently have been designed and tested to improve survival of patients with different cardiovascular diseases is provided.
3

Antisense oligonucleotides to PAI-1 mRNA as potential agents for therapeutic intervention in cardiovascular diseases

100%
Cierniewski C. S., Pawlowska Z., Pluskota E., Stasiak M., Kobylanska A., Misiura K., Maciaszek A., Koziolkiewicz M., Stec W. J.
Biotechnologia
|
1996
|
issue 4
141-152
EN
In this report we discuss the possibility of using antisense oligonucleotides specific to PAI-1 mRNA to reversibly decrease PAI-1 level in blood plasma and thus prolong a half-life time endogenous plasminogen activators in circulation.
4

From accuracy in protein synthesis to cardiovascular disease: the role of homocysteine

100%
Jakubowski H.
|
EN
The non-protein amino acid homocysteine (Hcy) enters the first step of protein synthesis and forms an aminoacyl-tRNA synthetase-bound homocysteinyl adenylate (Hcy-AMP). Direct incorporation of Hcy into tRNA and protein is prevented by editing activities of aminoacyl-tRNA synthetases that convert Hcy-AMP into Hcy thiolactone. Editing of Hcy occurs in all cell types investigated, including human. S-Nitrosylation of Hcy prevents its editing by MetRS and allows formation of S-nitroso-Hcy-tRNAMet, as well as incorporation of Hcy into proteins at positions specified by methionine codons. This provides an example of how the genetic code can be expanded by invasion of the metionine coding pathway by Hcy. Hcy can also be incorporated into protein post-translationally by a facile reaction of Hcy thiolactone with ?-amino groups of protein lysine residues. Hcy is present in human blood proteins, such as hemoglobin, serum albumin, and ?-globulins. Hcy thiolactonase, a component of high-density lipoprotein, minimizes protein N-homocysteinylation. Incorporation of Hcy into protein provides plausible chemical mechanism by which elevated levels of Hcy contribute to human cardiovascular disease.
5

Homocysteine, MTHFR gene polymorphisms, and cardio-cerebrovascular risk

75%
Trabetti E.
Journal of Applied Genetics
|
2008
|
vol. 49
|
issue 3
267-282
EN
Vascular diseases are commonly associated with traditional risk factors, but in the last decade scientific evidence has suggested that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischaemic events. Cardio- and cerebrovascular diseases are multifactorial, as their aetiopathogenesis is determined by genetic and environmental factors and by gene-gene and gene-environment interactions. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Hyperhomocysteinaemia may confer a mild risk alone, but it increases the risk of disease in association with other factors promoting vascular lesions. Variants in genes encoding enzymes involved in homocysteine metabolism, or depletion of important cofactors or substrates for those enzymes, including folate, vitamin B12 and vitamin B6, may result in elevated plasma homocysteine levels. Several studies have been performed to elucidate the genetic determinant of hyperhomocysteinaemia in patients with vascular disease, and the MTHFR 677C>T polymorphism is the one most extensively investigated. However, the lack of homogeneity in the data and the high number of factors influencing plasma homocysteine concentrations remain conflicting. Moreover, studies on the evaluation of therapeutic interventions in improving the atherogenic profile, lowering plasma homocysteine levels, and preventing vascular events, have shown inconsistent results, which are reviewed in this paper. More prospective, double-blind, randomized studies, including folate and vitamin B interventions, and genotyping for polymorphisms in genes involved in homocysteine metabolism, might better define the relationship between mild hyperhomocysteinaemia and vascular damage.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.