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<title>The Moldovan Medical Journal, Vol. 60, No 2, April 2017</title>
<link href="http://repository.usmf.md:80/xmlui/handle/20.500.12710/16081" rel="alternate"/>
<subtitle/>
<id>http://repository.usmf.md:80/xmlui/handle/20.500.12710/16081</id>
<updated>2026-04-19T01:10:50Z</updated>
<dc:date>2026-04-19T01:10:50Z</dc:date>
<entry>
<title>The Moldovan Medical Journal. April 2017, Vol. 60, No 2</title>
<link href="http://repository.usmf.md:80/xmlui/handle/20.500.12710/16256" rel="alternate"/>
<author>
<name/>
</author>
<id>http://repository.usmf.md:80/xmlui/handle/20.500.12710/16256</id>
<updated>2021-09-27T06:42:11Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">The Moldovan Medical Journal. April 2017, Vol. 60, No 2
The journal was founded in 1958 on the initiative of Nicolae Testemitsanu, an outstanding expert in orthopedics, social medicine, and public health. Now the publisher of the journal is the Scientific Medical Association of Moldova and the journal has become the scientific peer-reviewed periodical Edition designed for specialists in the areas of medicine, dentistry, pharmacy, social medicine, and public health. From its debut the journal has striven to support the interests of Moldovan medicine concerning the new concepts of its development. The aim of the Moldovan Medical Journal is to provide the international community with the results of scientific researches performed in the medical institutions of Moldova and inform Moldovan medical society about the advanced achievements of medicine abroad. The Editorial Board warmly welcomes both the readers of and the authors of the journal, all those who are enthusiastic about searching for new and more effective ways of solving numerous medical problems. We hope that those who want to make their contribution to the science of medicine will find our journal helpful and encouraging.
Fondatori: Ministerul Sănătăţii al Republicii Moldova, Universitatea de Stat de Medicină şi Farmacie “Nicolae Testemiţanu”
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Monograph “Pituitary adenomas. Morphopathology and molecular profile”, the author: Eugen Melnic</title>
<link href="http://repository.usmf.md:80/xmlui/handle/20.500.12710/14061" rel="alternate"/>
<author>
<name>Vataman, Vladimir</name>
</author>
<id>http://repository.usmf.md:80/xmlui/handle/20.500.12710/14061</id>
<updated>2021-09-27T06:42:30Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">Monograph “Pituitary adenomas. Morphopathology and molecular profile”, the author: Eugen Melnic
Vataman, Vladimir
Department of Morphopathology, Nicolae Testemitsanu State University of Medicine and Pharmacy, Chisinau, the Republic of Moldova
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>The role of homocysteine in endothelial dysfunction</title>
<link href="http://repository.usmf.md:80/xmlui/handle/20.500.12710/2719" rel="alternate"/>
<author>
<name>Visternicean, Elena</name>
</author>
<id>http://repository.usmf.md:80/xmlui/handle/20.500.12710/2719</id>
<updated>2021-09-27T06:44:04Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">The role of homocysteine in endothelial dysfunction
Visternicean, Elena
Background: Homocysteine is a sulfur-containing intermediate product in the normal metabolism of methionine, an essential amino acid.&#13;
Hyperhomocysteinemia defines the state in which concentrations of homocysteine exceeds normal level. Homocysteine is located at a metabolic branch&#13;
point and can either be irreversibly degraded to cysteine via the transsulfuration pathway, or conserved by remethylation back to methionine. Folic&#13;
acid, vitamin B12, and vitamin B6 deficiencies and reduced enzyme activities inhibit the breakdown of homocysteine, thus increasing the concentration&#13;
of intracellular homocysteine. Being cytotoxic, homocysteine is increasingly exported from the cell to become detectable in plasma. In recent years the&#13;
amino acid homocysteine has achieved the status of an important factor in vascular disease, diseases of aging, and other fundamental processes in biology&#13;
and medicine. Hyperhomocysteinemia may alter vascular morphology, stimulate inflammation, activate the endothelium and the blood clotting cascade,&#13;
and inhibit fibrinolysis. As a result, hyperhomocysteinemia is associated with loss of endothelial antithrombotic function and induction of a procoagulant&#13;
environment. The role of homocysteine in endothelial dysfunction is thought to be mediated by mechanisms including oxidative stress. Vascular injury&#13;
could be caused by an imbalance between nitric oxide production from dysfunctional endothelial cells and homocysteine concentrations.&#13;
Conclusions: Hyperhomocysteinemia is associated with alterations in vascular morphology, loss of endothelial antithrombotic function, and induction&#13;
of a procoagulant environment.
Department of Obstetrics and Gynecology No 2, Nicolae Testemitsanu State University of Medicine and Pharmacy, Chisinau, the Republic of Moldova
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Traumeel S – bioregulatory approach in the treatment of inflammation</title>
<link href="http://repository.usmf.md:80/xmlui/handle/20.500.12710/2721" rel="alternate"/>
<author>
<name>Popovich, S. V</name>
</author>
<author>
<name>Katerenchuk, I. P</name>
</author>
<id>http://repository.usmf.md:80/xmlui/handle/20.500.12710/2721</id>
<updated>2021-09-27T07:20:06Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">Traumeel S – bioregulatory approach in the treatment of inflammation
Popovich, S. V; Katerenchuk, I. P
Background: In the treatment of inflammation, the action of widely used non-steroidal anti-inflammatory drugs (NSAIDs) is directed mainly to inhibit&#13;
the synthesis of proinflammatory mediators, cell migration and proliferation, as well as to stimulate the formation of anti-inflammatory agents. These&#13;
effects allow to quickly and significantly limit the severe symptoms of acute inflammation and pain. However, at the same time, NSAIDs suppress the&#13;
sanogenetic mechanism of inflammation. Absence of correction of pathogenetic mechanisms of inflammation can lead to chronic inflammation and&#13;
development of its complications (cicatricial changes, adhesions, contractures, etc.). Also, nonselectivity of NSAIDs contributes to the development of&#13;
known side effects. And inhibitors of cyclooxygenase 2, as it became known, with excess daily therapeutic dose also cause serious side effects. New&#13;
possibilities for solving this problem have already been demonstrated by the bioregulatory approach and the complex bioregulatory medicines (BRMs)&#13;
created on its principles.&#13;
Conclusions: The complex bioregulatory action of the medicine Traumeel S allows to control and optimize the course of the inflammatory process wherever&#13;
it is located and of any form. Its use contributes to the full completion of inflammation with the recovery of the structure and function of the tissue,&#13;
reduces the risk of complications and chronic inflammation. Such characteristics, combined with good tolerability (absence of side effects characteristic&#13;
to NSAIDs) make Traumeel S a simple and reliable assistant to a doctor of any specialty in the treatment of inflammatory diseases of different localization.
Department of Research, Ukrainian Academy of Biological Medicine, Kiev, Ukraine, Department of Internal Medicine, Ukrainian Medical Dental Academy, Poltava, Ukraine
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
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