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The article presents the results of ultrastructural research on fibroblastic sarcoid, which is one of the most aggressive types of sarcoid in horses. A retrospective study on the prevalence of sarcoids in horses in Ukraine’s western regions was conducted in 2019–2023. It was found that during the period of 2022–2023, the number of horses with sarcoids increased sharply by 15.6% compared to the period 2020–2021. This was associated with the mass movement of animals from eastern regions due to the onset of the war in Ukraine. The fibroblastic type of sarcoid was predominantly localized in the abdominal wall and groin area. To study the ultrastructure of sarcoids, they were surgically removed by excising undamaged skin portions under general anesthesia, adhering to all requirements of the European Convention for the Protection of Animals used for Experimental and Other Scientific Purposes. Electronograms revealed that the tumour formation mainly consisted of fibroblasts of varying differentiation degrees: significant number of vesicles, markedly expanded endoplasmic reticulum cisterns, and irregularly shaped nuclei with numerous invaginations. Open nuclear pores were observed in most nuclei. Active formation of a large number of capillaries was noted between the collagen matrix, fibroblasts, and fibrocytes, indicated by the increased number of endotheliocytes with pseudopodia on the cytoplasm’s marginal part and the basal surface. This suggests their embryonic type. Endotheliocytes contained large round nuclei and a significant number of mitochondria in the cytoplasm. There were both bright and dark endotheliocytes in the blood capillaries’ venous section. The cytoplasm of bright endotheliocytes contained myofilaments, individual mitochondria, free ribosomes, peroxisomes, and vesicles of various sizes. The plasmalemma formed small pseudopodia. The capillary lumen showed moderate electron density. Additionally, high platelet activity was observed, manifested by cell adhesion to the marginal part of the endotheliocyte cytoplasm. It should be noted that most capillaries were of the venous type, as indicated by the endotheliocytes’ height, the presence of an increased number of mitochondria and vesicles. The entire cellular pool was localized among the massive framework consisting of collagen fibers. Elastic fibers could not be detected in the fibrillar component.

The article presents the results of ultrastructural research on fibroblastic sarcoid, which is one of the most aggressive types of sarcoid in horses. A retrospective study on the prevalence of sarcoids in horses in Ukraine’s western regions was conducted in 2019–2023. It was found that during the period of 2022–2023, the number of horses with sarcoids increased sharply by 15.6% compared to the period 2020–2021. This was associated with the mass movement of animals from eastern regions due to the onset of the war in Ukraine. The fibroblastic type of sarcoid was predominantly localized in the abdominal wall and groin area. To study the ultrastructure of sarcoids, they were surgically removed by excising undamaged skin portions under general anesthesia, adhering to all requirements of the European Convention for the Protection of Animals used for Experimental and Other Scientific Purposes. Electronograms revealed that the tumour formation mainly consisted of fibroblasts of varying differentiation degrees: significant number of vesicles, markedly expanded endoplasmic reticulum cisterns, and irregularly shaped nuclei with numerous invaginations. Open nuclear pores were observed in most nuclei. Active formation of a large number of capillaries was noted between the collagen matrix, fibroblasts, and fibrocytes, indicated by the increased number of endotheliocytes with pseudopodia on the cytoplasm’s marginal part and the basal surface. This suggests their embryonic type. Endotheliocytes contained large round nuclei and a significant number of mitochondria in the cytoplasm. There were both bright and dark endotheliocytes in the blood capillaries’ venous section. The cytoplasm of bright endotheliocytes contained myofilaments, individual mitochondria, free ribosomes, peroxisomes, and vesicles of various sizes. The plasmalemma formed small pseudopodia. The capillary lumen showed moderate electron density. Additionally, high platelet activity was observed, manifested by cell adhesion to the marginal part of the endotheliocyte cytoplasm. It should be noted that most capillaries were of the venous type, as indicated by the endotheliocytes’ height, the presence of an increased number of mitochondria and vesicles. The entire cellular pool was localized among the massive framework consisting of collagen fibers. Elastic fibers could not be detected in the fibrillar component. [ABSTRACT FROM AUTHOR]

Heparin-induced thrombocytopenia type II (HIT II), as stated in the literature, occurs in about 3% of all patients and in 0.1–5% of surgical patients. Thrombosis develops in 20–64% of patients with HIT. The mortality rate in HIT II has not decreased using non-heparin treatment with anticoagulants such as argatroban and lepirudin. An improved understanding of the pathophysiology of HIT may help identify targeted therapies to prevent thrombosis without subjecting patients to the risk of intense anticoagulation. The review will summarize the current knowledge about the pathogenesis of HIT II, potential new therapeutic targets related to it, and new treatments being developed. HIT II pathogenesis involves multi-step immune-mediated pathways dependent on the ratio of PF4/heparin and platelet, monocyte, neutrophil, and endothelium activation. For years, only platelets were known to take part in HIT II development. A few years ago, specific receptors and signal-induced pathways in monocytes, neutrophils and endothelium were revealed. It had been shown that the cells that had become active realised different newly formed compounds (platelet-released TF, TNFα, NAP2, CXCL-7, ENA-78, platelet-derived microparticles; monocytes-TF-MPs; neutrophils-NETs), leading to additional cell activation and consequently thrombin generation, resulting in thrombosis. Knowledge about FcγIIa receptors on platelets, monocytes, neutrophils and FcγIIIa on endothelium, chemokine (CXCR-2), and PSGL-1 receptors on neutrophils could allow for the development of a new non-anticoagulant treatment for HIT II. IgG degradation, Syk kinase and NETosis inhibition are in the field of developing new treatment possibilities too. Accordingly, IdeS and DNases-related pathways should be investigated for better understanding of HIT pathogenesis and the possibilities of being the HIT II treatment targets. [ABSTRACT FROM AUTHOR]

It is known that mitochondrial dysfunction can be a trigger or a concomitant mechanism in the development of Alzheimer's disease. It is also known that the restoration of intracellular mitochondrial activity of neurons and cerebral endotheliocytes is possible due to the transfer of intact mitochondria from other brain cells—in particular, astrocytes—and this transfer of mitochondria is mediated by the CD38 protein and functionally linked to it connexin 43 (Cx43). It follows that these molecules are promising for study both in relation to the mechanisms of development of neurodegeneration and in relation to the possible modulation of their activity for the correction of neurological deficits. The aim of this work was to study changes in the number of CD38- and Cx43-immunopositive cells in the neurovascular unit and the blood–brain barrier (BBB) of the brain in experimental Alzheimer's disease. We have shown that the toxic effect of β-amyloid leads to a significant increase in the number of CD38- and Cx43-positive cells as in the hippocampus of animals in vivo, and as part of the BBB model in vitro. We have also shown that the cultivation of isolated astrocytes in the presence of β-amyloid leads to an increase in the content of Cx43 in cells and that the permeability of these half-channels significantly increases. [ABSTRACT FROM AUTHOR]

Objective: Mechanical trauma to the testicles poses a potential risk of tissue destruction, disruption of local blood supply, and impairment of spermatogenesis, which can ultimately lead to infertility. Therefore, investigating this topic is crucial. The study aimed to identify cytological and morphological changes in the testicular tissue of laboratory rats following mechanical trauma to the organ., Methods: Observations were recorded on days 7, 14, 30, and 90 post-trauma. The experiment involved two groups of animals: a control group of healthy animals and an experimental group that sustained blunt mechanical trauma. Tissue samples were collected, fixed, dehydrated, and embedded in paraffin; subsequently, sections were prepared and stained. Structural changes in tissues and cells were documented using light and transmission electron microscopy., Results: In the experimental sample, notable changes included a decrease in organ weight, thickening of the protein shell and tubule walls, sclerotisation of the tubule membrane, narrowing of tubule diameter, reduced spermatozoa and spermatids titre, diminished capillary network and spermatogenic epithelium, uneven blood vessel lumen expansion, and decreased volume of Leydig cell nuclei. Additionally, in cells under different functional loads, the cytoplasm was vacuolated, mitochondrial cristae and the Golgi apparatus were diminished, cytoplasm volume decreased, karyopyknosis was observed, and uncharacteristic protrusions appeared on the surface of the cytoplasmic membrane. The severity of destruction at the cellular and tissue levels showed a positive correlation with time., Conclusion: The data obtained from these model sites can be predictive for clinical trials.

Irradiation with red or near-infrared (NIR) light in low level light therapy (LLLT) is found to stimulate cellular processes and bioenergetics, resulting in enhanced wound healing, pain control, neurodegenerative diseases treatment, etc. During light irradiation of tissues and organs, different cells are affected, though the connection between photostimulation of cells and their environmental conditions remains poorly understood. In this report, red/NIR light-stimulated angiogenesis is investigated using endothelial cells in vitro, with a focus on the capillary-like structure (CLS) formation and the respective biochemical processes in cells under conditions proximate to a healthy or malignant environment, which strongly defines angiogenesis. To model environmental conditions for endotheliocytes in vitro, the cell culture environment was supplemented by an augmented conditioned medium from macrophages or cancer cells. The biochemical processes in endothelial cell cultures were investigated with and without irradiation by red (650 nm) and near-infrared (808 nm) laser diodes and under normoxia or hypoxia conditions. A light-stimulated angiogenesis has been found, with a more efficient stimulation by 650 nm light compared to 808 nm light. It was shown that the irradiation with light promoted extracellular Ca2+ influx, fostered cell cycle progression, proliferation and NO generation in endothelial cells, and caused an increase in vascular endothelial growth factor (VEGF) production by endothelial cells and M2 macrophages under hypoxia conditions. The activation of VEGF production by macrophages was found to be associated with an increase in the number of M2 macrophages after light irradiation under hypoxia conditions. Thus, a new pathway of an activation of the endothelial cell metabolism, which is related with the extracellular Ca2+ influx after light irradiation, has been revealed. Red/NIR light-stimulated angiogenesis has been studied using endothelial cells in vitro, with focus on CLS formation and the respective biochemical processes in cell models proximate to a healthy or malignant environment. A light-stimulated angiogenesis has been found, stimulated via extracellular Ca2+ influx, cell cycle progression, proliferation and NO generation, VEGF production increase by endothelial cells under hypoxia conditions. [Display omitted] • Red and near-infrared light stimulates angiogenesis in vitro, with more efficient stimulation at 650 nm than 808 nm. • The irradiation promotes Ca ion influx, cell cycle progression, proliferation, and NO generation in endothelial cells. • The irradiation increases VEGF production by endothelial cells and macrophages under hypoxia. • An increase in VEGF production is associated with a rise in the number of M2 macrophages after irradiation under hypoxia. • A new activation pathway of endothelial cell metabolism, which is related to light-induced Ca ion influx, is revealed. [ABSTRACT FROM AUTHOR]