Pathophysiological mechanisms and consequences of cardiovascular calcifications: Role of uremic toxicity

Purpose. To analyze the results of classical and modern studies reflecting the pathophysiological mechanisms of antipsychotic-induced tardive dyskinesia.Materials and methods. We searched for full-text publications in Russian and English in the databases of E-Library, PubMed, Web of Science and Springer published over the past decade, using keywords (tardive dyskinesia (TD), drug-induced tardive dyskinesia, antipsychotics (AP), neuroleptics, typical antipsychotics, atypical antipsychotics, pathophysiology, etiology and combinations of these words). In addition, the review included earlier publications of historical interest.Results. The lecture proposed theories of development of AP-induced TD, examining its effect on dopaminergic receptors, dopaminergic neurons, neurons of the basal ganglia, and other theories: activation of estrogen receptors, disorders of melatonin metabolism, disorders of the endogenous opioid system, oxidative stress with predominant oxidation processes, blockade of 5-HT2-receptors, a decrease in the pyridoxine level, genetic predisposition, interaction of AP with the brain trace element – iron, carbonyl stress and immune inflammation and the role of the neurotrophic factor.Conclusion. The disclosure of the mechanisms of AP-induced TD will allow the development of a strategy for personalized prevention and therapy of the considered neurological complication of the AP-therapy for schizophrenia in real clinical practice.

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Cardiac syndrome X. the possible role of Na+-Li+-countertransport activity and other pathophysiological mechanisms in pathogenesis

Kazan medical journal ◽

10.17816/kmj2184 ◽

2013 ◽

Vol 94 (3) ◽

pp. 355-361

Author(s):

V N Oslopov ◽

Y V Oslopova ◽

D V Borisov

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Vascular Dysfunction ◽

Syndrome X ◽

Cardiac Syndrome X ◽

Pathophysiological Mechanisms ◽

Cardiac Syndrome ◽

Number Of Patients

There are numerous pathophysiological mechanisms unequally responsible for the cardiac syndrome X development. The most important is endothelium and smooth muscle cells dysfunction that can intensify vasoconstriction and depress both endothelium-dependant and endothelium-independent vasodilatation, finally leading to coronary micro vascular dysfunction as the basis of the cardiac syndrome X pathogenesis. Together with other possible mechanisms of pathogenesis, studying the importance of increased cell membrane Na+-Li+-countertransport activity seems promising. If was found that a significant number of patients with cardiac syndrome X have increased Na+-Li+-countertransport activity, which is an in vitro marker of Na+-H+-antiporter. Therefore, it is important to measure Na+-Li+-countertransport speed in patients with coronary heart disease, because its high levels increases the chance for cardiac syndrome X, which is a coronary heart disease with no anatomic signs of coronary arteries involvement.

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The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/8877116 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9

Author(s):

M. Jelinek ◽

M. Jurajda ◽

K. Duris

Keyword(s):

Oxidative Stress ◽

Free Radicals ◽

Subarachnoid Hemorrhage ◽

Brain Injury ◽

Molecular Mechanisms ◽

Early Brain Injury ◽

Pathophysiological Mechanisms ◽

Spontaneous Subarachnoid Hemorrhage ◽

Antioxidant Mechanisms

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals’ generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals’ generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

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Hemostasis Disturbances in Patients in the Acute Period of Isolated Traumatic Brain Injury (Review)

General Reanimatology ◽

10.15360/1813-9779-2018-5-85-95 ◽

2018 ◽

Vol 14 (5) ◽

pp. 85-95 ◽

Cited By ~ 2

Author(s):

A. I. Baranich ◽

A. A. Sychev ◽

I. А. Savin ◽

A. A. Polupan ◽

A. V. Oshorov ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Protein C ◽

Coagulation System ◽

Normal Functioning ◽

Secondary Brain Damage ◽

Pathophysiological Mechanisms ◽

The Brain ◽

Ischemic Events

Acute isolated traumatic brain injury (TBI) is frequently associated with occurrence of hemostasis disorders, which may be accompanied with hemorrhagic and ischemic events in the brain matter, hence, normal functioning of the blood coagulation system is critical. Understanding of the pathophysiological mechanisms of this phenomenon might help adequate prophylaxis of secondary brain damage. Earlier, development of disseminated intravascular coagulation syndrome (DIC) has been generally considered as a mechanism of coagulation disorders during TBI. However, over the recent decades, new data emerged concerning the key role of tissue factor, systemic inflammation response, thrombocytopathy, protein C effect in the occurrence of this coagulopathy. This overview of literature is aimed at providing the new data on specific pathophysiological mechanisms underlying coagulopathy following TBI.

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The role of neurokinin B in the pathophysiological mechanisms of vasomotor symptoms and sleep disorders in postmenopausal women

Maturitas ◽

10.1016/j.maturitas.2021.08.014 ◽

2021 ◽

Vol 152 ◽

pp. 69-70

Author(s):

Svetlana Yureneva ◽

Viktoriya Averkova ◽

Zuhra Ebzieva ◽

Tatyana Ivanets

Keyword(s):

Sleep Disorders ◽

Postmenopausal Women ◽

Vasomotor Symptoms ◽

Neurokinin B ◽

Pathophysiological Mechanisms

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Telangiectasias in Ataxia Telangiectasia: Clinical significance, role of ATM deficiency and potential pathophysiological mechanisms

European Journal of Medical Genetics ◽

10.1016/j.ejmg.2017.12.012 ◽

2018 ◽

Vol 61 (5) ◽

pp. 284-287 ◽

Cited By ~ 5

Author(s):

M.H.D. Schoenaker ◽

N.J.H. Van Os ◽

M. Van der Flier ◽

M. Van Deuren ◽

M.M. Seyger ◽

...

Keyword(s):

Clinical Significance ◽

Ataxia Telangiectasia ◽

Pathophysiological Mechanisms

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Molecular and Pathophysiological Mechanisms of Diabetic Retinopathy in Relation to Adhesion Molecules

Current Diabetes Reviews ◽

10.2174/1573399814666181017103844 ◽

2019 ◽

Vol 15 (5) ◽

pp. 363-371 ◽

Cited By ~ 3

Author(s):

Salini Scaria Joy ◽

Khalid Siddiqui

Keyword(s):

Diabetic Retinopathy ◽

Endothelial Cell ◽

Endothelial Function ◽

Adhesion Molecules ◽

Inflammatory Factors ◽

Low Grade ◽

Pathophysiological Mechanisms ◽

Low Grade Inflammation ◽

Slow Rolling

Diabetic Retinopathy (DR) is considered as a most common microvascular complication of diabetes affected by one in three people who are suffered for diabetes. Several pathophysiological mechanisms and adhesion molecules may play an etiologic role in the development of diabetes and its complications. The adhesion molecules located on both leucocytes and endothelial cells and considered as important molecules which can assessed the endothelial function. The functions of adhesion molecules involved in the cellular margination, slow rolling and transmigration of leukocytes. Hyperglycemia and its immediate biochemical sequelae or the low-grade inflammation directly alter endothelial function or influence endothelial cell functioning indirectly by induce oxidative stress and activates leukocytosis and leukocyte-endothelial cell interactions by the increased expression of adhesion molecules, growth factors, inflammatory factors, chemokines etc. and results DR. This review summarized the several pathophysiological mechanisms and role of adhesion molecules in disruption of homeostasis of vasculature by leukocytes in the development of diabetic retinopathy.

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Pathophysiological mechanisms in chronic musculoskeletal pain (fibromyalgia): the role of central and peripheral sensitization and pain disinhibition

Best Practice & Research Clinical Rheumatology ◽

10.1016/j.berh.2007.03.007 ◽

2007 ◽

Vol 21 (3) ◽

pp. 465-480 ◽

Cited By ~ 95

Author(s):

Lars Arendt Nielsen ◽

Karl G. Henriksson

Keyword(s):

Musculoskeletal Pain ◽

Chronic Musculoskeletal Pain ◽

Peripheral Sensitization ◽

Pathophysiological Mechanisms

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Malignant Pleural Effusion and Its Current Management: A Review

Medicina ◽

10.3390/medicina55080490 ◽

2019 ◽

Vol 55 (8) ◽

pp. 490 ◽

Cited By ~ 3

Author(s):

Skok ◽

Hladnik ◽

Grm ◽

Crnjac

Keyword(s):

Pleural Effusion ◽

Malignant Pleural Effusion ◽

Treatment Guidelines ◽

Medical Condition ◽

Molecular Techniques ◽

Treatment Modalities ◽

Common Symptom ◽

Advanced Malignancy ◽

Pathophysiological Mechanisms

Malignant pleural effusion (MPE) is an exudative effusion with malignant cells. MPE is a common symptom and accompanying manifestation of metastatic disease. It affects up to 15% of all patients with cancer and is the most common in lung, breast cancer, lymphoma, gynecological malignancies and malignant mesothelioma. In the last year, many studies were performed focusing on the pathophysiological mechanisms of MPE. With the advancement in molecular techniques, the importance of tumor-host cell interactions is becoming more apparent. Additionally, the process of pathogenesis is greatly affected by activating mutations of EGFR, KRAS, PIK3CA, BRAF, MET, EML4/ALK and RET, which correlate with an increased incidence of MPE. Considering all these changes, the authors aim to present a literature review of the newest findings, review of the guidelines and pathophysiological novelties in this field. Review of the just recently, after seven years published, practice guidelines, as well as analysis of more than 70 articles from the Pubmed, Medline databases that were almost exclusively published in indexed journals in the last few years, have relevance and contribute to the better understanding of the presented topic. MPE still presents a severe medical condition in patients with advanced malignancy. Recent findings in the field of pathophysiological mechanisms of MPE emphasize the role of molecular factors and mutations in the dynamics of the disease and its prognosis. Treatment guidelines offer a patient-centric approach with the use of new scoring systems, an out of hospital approach and ultrasound. The current guidelines address multiple areas of interest bring novelties in the form of validated prediction tools and can, based on evidence, improve patient outcomes. However, the role of biomarkers in a clinical setting, possible new treatment modalities and certain specific situations still present a challenge for new research.

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