1,203 results match your criteria: "Institute of General Pathology and Pathophysiology[Affiliation]"

The Expert Council has developed an algorithm for the diagnosis, treatment, and follow-up of patients with diabetes mellitus complicated by diabetic polyneuropathy (DPN), intended for use in both outpatient and inpatient settings. Particular emphasis is placed on the importance of early detection of DPN and interdisciplinary collaboration among specialists. The proposed algorithm includes recommendations for screening, clinical and instrumental diagnostics, risk stratification, and therapy selection based on the neuropathy phenotype, as well as the staged application of pathogenetic and symptomatic treatments, criteria for evaluating effectiveness, and indications for therapy continuation or adjustment.

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Autonomic disorders, including changes in heart rate, blood pressure, and respiration parameters, are some of the clinical manifestations of epileptic seizures, and their nature and severity may provide information about the localization of the epileptic focus. The origin of seizures from specific cortical structures of the brain, which belong to the central autonomic network and are involved in the autonomic regulation of vital functions, is often accompanied by typical changes in systemic hemodynamics and respiration; however, the pathogenesis of these processes is poorly understood. Modern approaches to examining patients with epilepsy, particularly the implantation of depth electrodes and direct cortical electrical stimulation of brain regions involved in autonomic regulation, enable the study of autonomic changes during an epileptic seizure with a direct connection to the studied cortical structure.

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Immunological correction of cognitive processes impaired due to the action of neurotoxic amyloidogenic forms of proinflammatory protein S100A9, a promoter of the inflammatory-amyloid cascade occurring in Alzheimer's disease, is poorly understood. Chronic intranasal administration of S100A9 fibrils leads to suppression of spatial memory formation in the Morris water maze in 12-month-old C57BL/6J mice and to an increase in activity of the ASCL1 gene involved in neurogenesis at the stage of cell differentiation, in the hippocampus and prefrontal cortex. In the case of combined administration of S100A9 fibrillar structures and antibodies to glutamate, the duration of the latency of reaching the platform in the water maze as well as ASCL1 gene expression in the hippocampus and prefrontal cortex returned to normal, but not in the cerebellum where a decrease in ASCL1 gene activity was observed.

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The discovery of a class of long noncoding RNAs (lncRNAs), including lncRNAs of the small nucleolar RNA (snoRNA) host gene family, SNHG, has led to growing interest in the study of both snoRNAs themselves and the genes encoding them. Currently, of the 232 known snoRNA genes, only 32 have been confirmed to have lncRNAs. At the same time, a positive correlation has been shown between the expression of lncRNAs and snoRNAs encoded by a common host gene of the SNHG family.

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Autoimmunity arises when the immune system erroneously attacks self-antigens, potentially resulting in organ dysfunction. This review focuses on the proliferation-inducing ligand, APRIL, and its critical role in regulating antibody-producing B cells. We explore the implications of APRIL in autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, and Sjögren's syndrome.

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The purpose of this work was to study the effects of lactoferrin (Lf) on acute (days 3 and 15) and early-delayed (day 30) changes in the dentate gyrus of mouse hippocampus caused by whole-body gamma-irradiation. Male C57BL/6 mice received Lf (4 mg per mouse, i.p.

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Neutrophil extracellular traps (NET) have emerged as critical players in the pathogenesis of atherosclerosis and other cardiovascular diseases (CVD). These web-like structures, composed of DNA, histones, and granule proteins released by neutrophils, contribute significantly to both inflammation and thrombosis. This manuscript offers a comprehensive review of the recent literature on the involvement of NET in atherosclerosis, highlighting their interactions with various pathophysiological processes and their potential as biomarkers for CVD.

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Eosinophils are multifunctional granulocytes that contribute to the initiation and modulation of inflammation. Accumulating evidence suggests that eosinophils are adaptable leukocytes that orchestrate the resolution of inflammatory responses. The most prevalent chronic inflammatory illness, rheumatoid arthritis (RA), is typified by persistent synovitis that makes it hard for the disease to go away on its own.

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Objective: To evaluate the efficacy and safety of combined therapy with lornoxicam (Xefokam Rapid) and a nucleotide complex Xefomielyn compared to lornoxicam monotherapy in patients with exacerbation of chronic nonspecific low back pain (CNLBP).

Material And Methods: The study included 181 patients divided into a monotherapy group Xefokam Rapid and a combined therapy group with the addition of the nucleotide complex Xefomielyn. Pain intensity was assessed using the Numerical Rating Scale, functional status using the Roland-Morris Disability Questionnaire, recurrence rate, and treatment satisfaction.

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Introduction: Postoperative hemorrhoidectomy wounds are prone to inflammation and microbial infection due to their anatomical location, necessitating effective therapeutic strategies. Chloramphenicol (CHL) is a broad-spectrum antibiotic with potential anti-inflammatory properties via Toll-like receptor 4 (TLR4) inhibition. This clinico- computational cohort study investigates CHL's dual therapeutic mechanism in postoperative hemorrhoid management, combining clinical outcomes with molecular modeling to elucidate its anti-inflammatory and antimicrobial effects.

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Inhibition of mitophagy is one of the signs of chronic disease pathogenesis. Detection and measurement of mitophagy levels under in vitro and in vivo models provide a better understanding of the role of mitophagy disorder in disease development and serve as prerequisites for creating a clinically applicable system test. The development of such a system is potentially feasible, but taking into account a number of factors that will be discussed in detail in this article.

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Rheumatoid arthritis (RA), a chronic autoimmune disease, is one of the major research themes in medicine. The current therapies have their limitations and cannot completely cure RA, but new therapeutic strategies are being proposed to reduce the shortcomings of approved drugs. This review will consider new potential treatment strategies for RA, including T-cell therapy, genetic editing and epigenetic regulation, what advantages and disadvantages they have and to what pathological target in RA they are directed.

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Atherosclerosis remains a leading cause of cardiovascular morbidity and mortality worldwide, underlying major conditions such as coronary heart disease and stroke. The pathogenesis of atherosclerosis is tightly linked to chronic inflammation and dysregulated lipid metabolism, processes that are also implicated in other inflammatory diseases like rheumatoid arthritis and psoriasis. Monoclonal antibodies (mAbs) have emerged as a promising therapeutic strategy, offering targeted intervention against key molecular drivers of atherosclerosis.

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It is well known that aqueous solutions can emit electromagnetic waves in the radio frequency range. However, the physical nature of this process is not yet fully understood. In this work, the possible role of gas nanobubbles formed in the bulk liquid is considered.

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The GABA receptors, through a short-term interaction with a mediator, induce hyperpolarization of the membrane potential () via the passive influx of chloride ions (Cl) into neurons. The massive (or intense) activation of the GABARs by the agonist could potentially lead to depolarization/excitation of the . Although the ionic mechanisms of GABA-mediated depolarization remain incompletely understood, a combination of the outward chloride current and the inward bicarbonate current and the resulting pH shift are the main reasons for this event.

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Fullerenes and fullerenols exhibit antioxidant and anti-inflammatory properties, making them promising candidates for Alzheimer's disease (AD) therapy. Unlike conventional anti-inflammatory drugs, these compounds have multitargeted effects, including their ability to inhibit amyloid fibril formation. However, few studies have explored their efficacy in high-validity AD models.

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Rheumatoid arthritis significantly increases the risk of cardiovascular disease due to chronic inflammation. This review's purpose is to critically analyze the intricate relationship between rheumatoid arthritis and cardiovascular disease, highlighting the mechanisms by which systemic inflammation contributes to cardiovascular risk and the effectiveness of current treatment strategies. We systematically evaluate existing literature on conventional cardiovascular risk factors in rheumatoid arthritis patients, as well as inflammation-specific markers that influence cardiovascular outcomes.

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We assessed the transcriptional activity of the genes PGC-1α, GR, SUCNR1, and SDHA in the cerebral cortex of old (age 18 months) male rats receiving course administration of dexamethasone alone and in combination with ethylmethylhydroxypyridine succinate. According to real-time PCR data, the course intraperitoneal administration of the glucocorticoid receptor (GRα) agonist dexamethasone (1 mg/kg, daily for 10 days) reduced the expression of the PGC-1α, GR, SUCNR1, and SDHA genes in rat cerebral cortex. Intraperitoneal administration of ethylmethylhydroxypyridine succinate (100 mg/kg, daily for 10 days) after each dexamethasone injection normalized the expression of PGC-1α and SUCNR1 genes and significantly activated the expression of GR and SDHA.

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Atherosclerosis is a complex cardiovascular disease characterised by the accumulation of lipids, inflammatory cells, and fibrous elements within arterial walls, leading to plaque formation and increased risk of cardiovascular events. Recent evidence highlights the pivotal roles of purinergic receptors in mediating the inflammatory and cellular processes associated with atherosclerosis. This review examines the roles of purinergic receptors in the pathophysiology of atherosclerosis, with a particular focus on the P1 subtype (A2A and A3 receptors), the P2X subtype (P2X4 and P2X7 receptors), and the P2Y subtype (P2Y2, P2Y11, and P2Y12 receptors).

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The uncontrolled fibrosis of lung tissue can lead to premature death in patients suffering from idiopathic pulmonary fibrosis (IPF), and it complicates the course of chronic obstructive pulmonary disease (COPD) and emphysema. It is also a risk factor for developing lung cancer. Antifibrotic drugs, such as nantedanib and pirfenidone, are able to slow down the progression of pulmonary fibrosis, but more effective treatment is still needed to reverse it.

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The clinical effectiveness of physical training in a cardiac rehabilitation program (CRP) was assessed in hypertensive (AH), post-myocardial infarction (MI) patients. 206 patients were randomized into a physically trained group (PhTG, n=102) and an untrained, control group (CG, n=104). All patients received standard drug therapy.

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Chimeric antigen receptor (CAR)-T cell therapy, a breakthrough in hematological cancer treatment, is now being explored for autoimmune diseases like rheumatoid arthritis (RA). RA, characterized by chronic joint inflammation and autoantibody production, presents a compelling target for CAR-T cell therapy due to its potential for precise targeting of aberrant immune cells and restoration of immune tolerance. This review analyzes current strategies in CAR-T cell therapy for RA, focusing on molecular mechanisms and clinical implications.

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Atherosclerosis, a chronic inflammatory disease, involves a complex interplay between endothelial cells, smooth muscle cells, and inflammatory mediators. Cell-to-cell junctions, including adherens junctions (AJs), tight junctions (TJs), and gap junctions (GJs), play a critical role in maintaining vascular integrity and regulating cellular interactions in the vascular wall. This review summarises the molecular mechanisms by which these junctions contribute to atherosclerosis, focusing on key proteins like VE-cadherin (AJs), ZO-1, occludin, and claudins (TJs), and connexins (GJs).

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