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        <rdf:li rdf:resource="http://dspace.zsmu.edu.ua/handle/123456789/26420" />
        <rdf:li rdf:resource="http://dspace.zsmu.edu.ua/handle/123456789/26419" />
        <rdf:li rdf:resource="http://dspace.zsmu.edu.ua/handle/123456789/26019" />
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    <dc:date>2026-11-15T05:29:51Z</dc:date>
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  <item rdf:about="http://dspace.zsmu.edu.ua/handle/123456789/26420">
    <title>The Role and Significance of Oxidative Stress in Inflammatory Periodontal Disease and Contemporary Approaches to Antioxidant Therapy</title>
    <link>http://dspace.zsmu.edu.ua/handle/123456789/26420</link>
    <description>Название: The Role and Significance of Oxidative Stress in Inflammatory Periodontal Disease and Contemporary Approaches to Antioxidant Therapy
Авторы: Belenichev, I.  F.; Popazova, O. O.; Salnykov, V.  I.; Bukhtiyarova, N. V.; Ryzhenko, V. P.; Petakh, P.; Kamyshny, O.; Oliynyk, S.; Lee, S.; Kyu-Ho, Yi; Бєленічев, Ігор Федорович; Попазова, Олена Олександрівна; Сальников, Валерій Ігорович; Бухтіярова, Ніна Вікторівна; Риженко, Віктор Павлович
Аннотация: Periodontitis is a chronic inflammatory disease driven by dysbiotic biofilms and an exaggerated host&#xD;
immune response, resulting in progressive destruction of periodontal tissues and tooth loss. Increasing&#xD;
evidence suggests that oxidative and nitrosative stress play central roles in disease progression by&#xD;
amplifying inflammation, promoting tissue damage, and impairing repair mechanisms.&#xD;
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) derived from immune cells, mitochondria,&#xD;
and enzymatic pathways contribute to lipid peroxidation, DNA damage, and alveolar bone resorption. These&#xD;
mechanisms help explain persistent inflammation and variable treatment response despite conventional&#xD;
periodontal therapy.&#xD;
This narrative review summarizes current evidence on oxidative stress in periodontitis and evaluates the&#xD;
potential role of antioxidant therapy as an adjunct to standard treatment. Particular emphasis is placed on&#xD;
selenium-containing compounds due to their involvement in glutathione peroxidase activity, thioredoxin&#xD;
systems, and mitochondrial protection.&#xD;
Although antioxidant strategies show promise in improving biochemical and clinical outcomes, current&#xD;
evidence remains heterogeneous. Further well-designed clinical studies are needed to clarify their role in&#xD;
routine periodontal care.</description>
    <dc:date>2026-01-01T00:00:00Z</dc:date>
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  <item rdf:about="http://dspace.zsmu.edu.ua/handle/123456789/26419">
    <title>Nitric Oxide and Mitochondrial Dysfunction in Chronic Heart Failure: A Narrative Review</title>
    <link>http://dspace.zsmu.edu.ua/handle/123456789/26419</link>
    <description>Название: Nitric Oxide and Mitochondrial Dysfunction in Chronic Heart Failure: A Narrative Review
Авторы: Belenichev, I.  F.; Aliyeva, O. H.; Bukhtiyarova, N. V.; Ryzhenko, V. P.; Kyuho, Yi; Бєленічев, Ігор Федорович; Алієва, Олена Геннадіївна; Бухтіярова, Ніна Вікторівна; Риженко, Віктор Павлович
Аннотация: Chronic heart failure (CHF) remains a leading cause of hospital admission, disability, and cardiovascular&#xD;
death despite major advances in guideline-directed therapy. Beyond hemodynamic impairment and&#xD;
neurohormonal activation, CHF is increasingly understood as a disorder of endothelial dysfunction, nitrosoredox&#xD;
imbalance, mitochondrial injury, energetic failure, and regulated cell death. Nitric oxide (NO)&#xD;
signaling and mitochondrial homeostasis are interconnected components of this broader pathophysiologic&#xD;
network. Under physiologic conditions, endothelial NO synthase-derived NO contributes to vascular tone,&#xD;
coronary microvascular regulation, and myocardial signaling. In CHF, reduced endothelial NO bioavailability&#xD;
may coexist with increased formation of reactive nitrogen species, particularly in inflammatory and&#xD;
oxidizing conditions. The resulting nitroso-redox imbalance can interact with mitochondrial respiratory&#xD;
dysfunction, altered calcium handling, oxidative stress, and regulated cell death, although the relative&#xD;
contribution of these mechanisms varies across heart failure phenotypes and disease states. Guidelinedirected&#xD;
therapies, including angiotensin-converting enzyme inhibitors, angiotensin receptor-neprilysin&#xD;
inhibitors, sodium-glucose cotransporter 2 inhibitors, evidence-based beta-blockers, and mineralocorticoid&#xD;
receptor antagonists, improve clinical outcomes through established neurohormonal, renal, and&#xD;
hemodynamic mechanisms. Experimental and translational evidence suggests that some of these therapies&#xD;
may also influence endothelial, redox, metabolic, or mitochondrial pathways, although the clinical&#xD;
contribution of these secondary effects remains incompletely defined. These mechanistic observations have&#xD;
also motivated investigation of therapies that more directly target endothelial, redox, or mitochondrial&#xD;
abnormalities. Hypertril (1-(beta-phenylethyl)-4-amino-1,2,4-triazolium bromide) is an investigational&#xD;
compound with reported beta-blocking, NO-related, and metabolic effects in experimental models;&#xD;
however, the available evidence remains predominantly preclinical and does not establish clinical efficacy in&#xD;
human CHF. This narrative review examines NO dysregulation and mitochondrial dysfunction as&#xD;
interconnected components of CHF pathophysiology, considers their relationship to contemporary&#xD;
pharmacotherapy, and discusses the translational limitations and research priorities associated with&#xD;
targeting these pathways.</description>
    <dc:date>2026-01-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://dspace.zsmu.edu.ua/handle/123456789/26019">
    <title>Cardioprotective Effects of Coupled SH/NO System Modulators in a Rat Model of Doxorubicin-Induced Heart Failure</title>
    <link>http://dspace.zsmu.edu.ua/handle/123456789/26019</link>
    <description>Название: Cardioprotective Effects of Coupled SH/NO System Modulators in a Rat Model of Doxorubicin-Induced Heart Failure
Авторы: Ryzhenko, V. P.; Belenichev, I. F.; Popazova, O. O.; Bukhtiyarova, N. V.; Oliynyk, S.; Petakh, P.; Halabitska, I.; Kamyshnyi, O.; Риженко, Віктор Павлович; Бєленічев, Ігор Федорович; Попазова, Олена Олександрівна; Бухтіярова, Ніна Вікторівна
Аннотация: Background: The high prevalence of chronic heart failure (CHF) in industrialized countries,&#xD;
alongside its grave consequences—including increased mortality, disability, functional&#xD;
impairment, and reduced quality of life—underscores the urgent need to optimize&#xD;
core medical therapy. In this regard, metabolic cardioprotectants are of particular interest,&#xD;
as their action is aimed at interrupting or mitigating the cascade of adverse metabolic reactions&#xD;
and enhancing the compensatory and adaptive mechanisms of the heart. The aim&#xD;
of this study was to evaluate the effect of sulfur-containing pharmacological agents—&#xD;
namely, N-acetylcysteine (NAC), Heptral, Thiotriazoline, and Angiolin—on selected parameters&#xD;
of the NO and thiol-disulfide systems in the hearts of rats with experimental&#xD;
doxorubicin-induced CHF, followed by an assessment of their cardioprotective efficacy</description>
    <dc:date>2026-01-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="http://dspace.zsmu.edu.ua/handle/123456789/26017">
    <title>Проведення практичних занять провізорам-слухачам курсів підвищення кваліфікації по ускладненням лікарської терапії</title>
    <link>http://dspace.zsmu.edu.ua/handle/123456789/26017</link>
    <description>Название: Проведення практичних занять провізорам-слухачам курсів підвищення кваліфікації по ускладненням лікарської терапії
Авторы: Білай, Іван Михайлович; Райкова, Т. С.; Демченко, B. О.; Рижов, Олексій Анатолійович; Пашко, О. Є.</description>
    <dc:date>2013-01-01T00:00:00Z</dc:date>
  </item>
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