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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]

The problem of postcovidal syndrome is currently relevant, since in the stabilization of vital functions, the processes of immunological inflammation with significant disorders of endothelium functions continue; this causes tissue ischemization, especially in the presence of changes at the level of microcirculation in patients with angiopathy and vasculopathy. It is noted that in COVID-19 comorbidity with hypertension, coronary heart disease, diabetes mellitus, systemic connective tissue diseases the risks, course, prognosis and development of vascular complications significantly increase. The severity of the inflammatory process and predicting the likelihood of complications is accompanied by changes in laboratory indicators, namely: in the general blood test – leukocytosis, an increase in the level of neitrophilic granulocytes, a decrease in the content of hemoglobin and platelets; in biochemical indicators – a decrease in the level of the general protein, an increase in the indicators of alaninetransferase, aspartaminotransferase, C-reactive protein, lactatdehydrogenase, ferritin; coagulation changes – increase in the level of fibrinogen, D-dimer, reduction of activated partial thromboplastic time. On the basis of the considered clinical cases, taking into account modern ideas about the peculiarities of the development of thrombotic complications in COVID-19 infection in patients with ischemic lesions of the extremities, the need to prescribe low molecular weight heparin as a selection drug for the treatment of thrombophilic conditions has been proven. Detailed study of histological material is important for establishing changes at the level of microcirculation and ischemization of tissues, this will allow to develop algorithms for the treatment and prevention of complications. Solving these issues, not only in the presence of COVID-19, but also in any stressful cases, requires careful clarification of the mechanisms for the development of complications and a timely adequate integrated approach to treatment to improve and stabilize the condition of patients.

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.

Microgravity is a component of the complex environment in space. Due to its adverse effects on the human body, it poses unknown obstacles to the implementation of space missions. In microgravity, the body often loses the point of force and it is difficult to control itself, which leads to various accidental collisions. As the largest organ of the human body, the skin is often damaged by traumatic injury because of its large contact area with the external environment. In this study, we summarized and discussed the latest research on the impact of weightlessness or simulated microgravity on the skin and the process of wound healing to further understand the changes and mechanisms of wound healing. A series of studies have investigated the effects of weightlessness or simulated microgravity on the human skin and the wound healing process. Under microgravity environment, the skin showed certain changes, such as thinning and altered blood supply; microgravity also affected various cellular functions and their associations with the extracellular matrix during wound healing. Various stages of wound healing and sophisticated interactions between the elements involved in wound healing become disordered in a microgravity environment. However, more studies are needed to further understand the impact and mechanisms of microgravity on the trauma repair process to provide theoretical guidance for wound healing. With the support and help of a lot of good researches and trails, accidental trauma will no longer be an obstacle to human exploration of space. [ABSTRACT FROM AUTHOR]

The sources of vascularization of the kidneys of five polar owl carcasses were studied by filling the vessels with self-hardening plastic Belokril through the femoral artery. High-grade oil paints were added to the monomer to give the vessels the desired color. After the injection, the carcasses were placed in a high concentration caustic soda solution for three days. The resulting corrosion impression was washed under warm water and dried. It was identified that in the lumbar trunk, the main vessel was the descending aorta, from which extra- and intraorganic arteries departed for vascularizing the kidneys. Extraorganic arteries included external and internal iliac, sciatic and middle sacral arteries. Intraorganic arteries included cranial, middle, and caudal renal arteries. Inside the parenchyma of each lobe of the kidney, intraorganic arteries branched in the main type of caudomedial, dorsomedial and lateromedial directions and were subdivided into segmental, interlobular and perilobular arteries and intralobular capillaries. An asymmetry in the branching of the renal arteries was observed. During histological examination, we noted that the renal arteries were lined with endothelium on the inner side and the intima contained endotheliocytes with oval nuclei. Under the endothelial layer were loose collagen fibers running along the middle shell. There was no loose connective tissue between the inner and middle shells, so the subendothelial layer was very weak and there was no internal elastic membrane. The muscle membrane was well developed, with collagen and elastic fibers located between the muscle fibers. The outer shell was represented by loose connective tissue with the presence of arterial and venous vessels. The collagen fibers had a slightly convoluted course. [ABSTRACT FROM AUTHOR]

Aim. To study the cytoprotective activity of peptides that mimic the spatial structure of the erythropoietin α-helix B in vitro. Material and methods. The experiment was performed on the primary cell culture of human endotheliocytes (HUVEC). Hydrogen peroxide (H2O2) was used to mimic oxidative stress. Cells were scattered in 96-well gelatin-coated plates with a density of 5 thousand cells per well. After 24 hours of incubation, the studied peptides were introduced - the basic peptide - Helix B surface peptide HBSP (QEQLERALNSS) and its derivatives EP-11-1 (UEHLERALNSS), EP-11-2 (UEQLERALNCS), EP-11-3 (UEQLERALNTS) in 3 concentrations - 5 μg/ml, 30 μg/ml and 50 μg/ml. Cell viability was measured using the MTT test. Results. Initial screening of the cytoprotective activity of innovative peptides that mimic the erythropoietin α-helix B in vitro was performed. Our results demonstrate that the original HBSP peptide and its derivatives EP-11-1, EP-11-2, EP-11-3 have a pronounced (p<0.05, compared with the control) cytoprotective effect. Derivatives EP-11-1, EP-11-2 does not differ from the base peptide HBSP in terms of the level of detected activity. When comparing the density of the formazan solution and the percentage of surviving endotheliocytes between the series of experiments with the base peptide HBSP and its derivatives, EP-11-3 showed significant superior cytoprotective effects when compared with HBSP (p<0.05), all over the entire range studied concentrations. Conclusion. Derivatives of the original peptide with laboratory code EP-11-1, EP-11-2 do not differ in their cytoprotective action from the base peptide HBSP. While the derivatives with laboratory code EP-11-3 presented a higher and significant cytoprotective activity when compared to the base peptide HBSP. [ABSTRACT FROM AUTHOR]

Bone marrow-derived mesenchymal stem cells (BMSCs) possess potential therapeutic properties for treating patients with chronic obstructive pulmonary disease (COPD), which is characterized by emphysema and obstructive sleep apnea (OSA). However, their effects on overlap syndrome (OS) remain unclear. We investigated the potential therapeutic effects and possible mechanisms of BMSC transplantation in OS rats. To generate the OS model in rats, the animals underwent daily exposure to cigarette smoke and intermittent hypoxia. BMSCs were intravenously injected into rats. At 4 weeks post-transplantation, the severity of emphysema was assessed by lung hematoxylin and eosin (H&E) staining. The levels of oxidative stress and the malondialdehyde (MDA) and superoxide dismutase (SOD) contents in serum and lung were detected. The apoptosis of alveolar septal cells was also detected by TUNEL assay. Finally, we determined the expression of CD31 and VWF in lung tissues by an immunohistochemical (IHC) assay. It was found that BMSCs were able to migrate to the injured lung and aorta tissues. In lung tissues, transplanted BMSCs, some of which had differentiated into endotheliocytes, were found in the alveolar walls. The mean linear intercept (MLI) and pathological scores were higher and the mean alveolar number (MAN) was lower in the OS group than these parameters in the control group. These values were significantly reduced in the OS+BMSC group compared to those in the OS group. The MDA content was decreased and SOD activity was increased in the OS+BMSC group compared to those in the OS group. The apoptotic index of alveolar wall cells in the OS group was higher than that in the OS+BMSC group. The expression levels of CD31 and VWF in alveolar wall cells in the OS group were lower than those in the OS+BMSC group. These results indicate that BMSCs may inhibit the progression of emphysema in the OS model by differentiating into endotheliocytes and suppressing the apoptosis of endotheliocytes and oxidative stress. There is a possibility that the release of growth factors and structural support may be a determinant for the regenerative effects observed following treatment with BMSCs. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cells (MSCs) are widely used in experimental research on cell therapy intended for the stimulation of repair processes in damaged tissues and organs. The present review summarizes the results of studies devoted to the possible directions of MSC differentiation after the transplantation of these cells into damaged nerves or special engineered structures of biological and artificial biodegradable materials that join the ends of a damaged nerve (nerve conduits). Data on exogenous MSC differentiation into Schwann cells, pericytes, smooth muscle cells, endotheliocytes, and other cell types are presented. Methods for preliminary MSC differentiation in vitro and examples of beneficial effects of these cells transplanted into damaged conductive nerves on nerve regeneration are given. The fate of exogenous MSCs placed into an unnatural biological niche remains poorly characterized and requires further studies, as emphasized in the review. [ABSTRACT FROM AUTHOR]

The possibility of sphingosine-1-phosphate production by induced pluripotent stem cells is examined to assess their potential in treatment of sepsis. The hematopoietic embryoid bodies were derived from the culture of 6-day-old differentiated induced pluripotent stem cells. These embryoid bodies secreted sphingosine-1-phosphate, an important bioactive lipid that regulates integrity of the pulmonary endothelial barrier, prevents elevation of its permeability, and impedes the formation of stress fibers in human endotheliocytes derived from umbilical vein. The data attest to potentiality of induced pluripotent stem cells in treatment of sepsis. [ABSTRACT FROM AUTHOR]

The study examined the myocardial ultrastructural alterations in rats maintained on various atherogenic diets. It revealed the complex ultrastructural alterations of cardiomyocytes and endotheliocytes (including the lytic and destructive changes of the intracellular organelles, upregulation of the autophagocytosis in the cardiomyocytes, and necrobiosis with apoptosis of endotheliocytes) reflecting the cytopathic features of circulating cholesterol and lipoproteins, whose elevation determined the intensity of destructive processes. The revealed peculiarities in the changes of lipid inclusions (their osmiophilic transformation) in cardiomyocytes can be provoked by entry of cholesterol into the cells and its further metabolic modifications. During moderate dyslipidemia, the cardiomyocytes demonstrated the ultrastructural signs of induction of intracellular regeneration (marked with the clusters of polysomes in the intermyofibrillar and subsarcolemmal spaces with appearance of neogenic myofilaments) and upregulated pinocytotic activity. In all cases, up-regulated autophagocytosis in cardiomyocytes was accompanied by accumulation of myelin- and vacuole-like structures in the intercellular spaces and capillary lumens paralleled with appearance of activated forms of macrophages and fibroblasts in the myocardium. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) plays an important role in metabolism. Consequently, every tissue of our body is affected by changes in concentrations of nitric oxide and its metabolites. Here we analyze phenotypic effects of NO and its metabolites in macrophages, NK-cells and lymphocytes that perform protection of the host organism against malignant tumors and intracellular pathogens. Immune system imbalance may result from misregulation of NO synthesis. Nitric oxide also plays an important role in endothelial dysfunction including inhibition of platelet adhesion and aggregation, vasoconstriction and vasodilation disorders of blood vessels, blood rheology changes and the development of atherosclerotic plaques. Thus an imbalance in the synthesis of nitric oxide in the vascular endothelium may be an early marker of lesions of various origins. [ABSTRACT FROM AUTHOR]

We studied the effect of IFNα-2b and IFNβ-1a on phasic and tonic contractions of isolated bovine mesenteric lymphatic vessels and nodes. IFNα-2b and IFNβ-1a in concentrations of 250-1000 U/ml produced dose-dependent negative chronotropic and inotropic effects on spontaneous phasic contractions and tonus of lymphatic vessels and nodes. In de-endothelialized lymphatic vessels and nodes, IFNα-2b and IFNβ-1a in the same concentrations had less pronounced inhibitory effect on spontaneous contraction and tonus. L-NAME (100 μM) and charybdotoxin (0.1 μM with 0.5 μM apamine) significantly attenuated the inhibitory effect of IFNα-2b on phasic and tonic contractions of lymph nodes. L-NAME (100 μM) and indomethacin (10 μM) significantly reduced the IFNα-2b-induced inhibitory effect on phasic and tonic contractions of lymph node. These results indicate that IFNα-2b and IFNβ-1a have a pronounced inhibitory effect on the phasic and tonic contractions of bovine mesenteric lymphatic vessels and nodes. The responses are endothelium-dependent and are determined by production of NO and endothelium-dependent hyperpolarizing factor by endotheliocytes in lymphatic vessels and by production of NO and prostacyclin by endotheliocytes in the lymphatic nodes. [ABSTRACT FROM AUTHOR]

The desquamation of endothelium of arteries, small veins and venules, the arteriolospasm and perivascular edematization of varying degrees of severity was established in histological preparations of different brain regions in case of diabetic encephalopathy. It was shown, that variation coefficients of optical density of stained nuclear chromatin of endotheliocytes in the vessels of brain microcirculation were reliably higher in case of diabetic encephalopathy as compared with corresponding indices of control group; this indicated the decrease of functional capability of these cells and the development of endothelial dysfunction.

Objective To explore the influence of different pressure of ultrasound-targeted microbubble destruction on the expression of inflammatory factor and vascular endothelial growth factor ( VEGF) in human umbilical vein endothelial cells (HUvE-12 cells). Methods We cultured HUvE-12 cells in the DMEM-F12 medium containing 1 xl07/mL micro­bubbles. HUvE-12 cells were divided into 5 groups exposed to different ultrasound pressure (0，1.0，2. 0，3. 0 and 4. 0 MPa). After 1.5 h of ultrasound exposure, we detected the expression of reactive oxygen species ( ROS) by using full-au­tomatic microplate reader. At 8 h after corresponding interventions, the cell viability, P-selectin and VEGF expression was determined by MTT, immunofluorescence and Western blotting, respectively. Additionally, ROS inhibitor (GSH) or P-se­lectin inhibitor (rPSLG-Ig) were added into the 2. 0 MPa group, and VEGF expression was determined by Western blot­ting, respectively. Results The cell viability presented to be no difference in the 1.0 MPa and 2. 0 MPa groups as com­pared with 0 MPa group (all P >0. 05) , while it decreased significantly in the 3. 0 MPa and 4. 0 MPa groups ( all P < 0.05). The expression of ROS, P-selectin and VEGF increased in the 1.0, 2.0, 3.0, and 4. 0 MPa groups as compared with that of the 0 MPa group (all P <0.05). No difference was found in the expression of ROS, P-selectin and VEGF be­tween the 4. 0 MPa and 3. 0 MPa groups (all P >0. 05) . When GSH or rPSLG-Ig were added in the 2. 0 MPa group , the expression of VEGF was inhibited significantly as compared with that of 2. 0 MPa applied only ( all P < 0. 05 ) . Conclusion Ultrasound-targeted microbubble destruction can increase the expression of VEGF through inducing inflammatory reaction and promote angiogenesis, and 2. 0 MPa is the optimal ultrasound pressure. [ABSTRACT FROM AUTHOR]

Under some pathological conditions, the natural dicarbonyl compounds can accumulate in the blood. The examples are malonyldialdehyde (MDA) formed as a secondary product of lipid peroxidation of unsaturated fatty acids during atherosclerosis, and glyoxal (GOX), a homolog of MDA, which accumulates during glucose autoxidation in patients with diabetes mellitus. This study compared the influence of both dicarbonyl compounds on low-density lipoproteins (LDL) and the membrane of endotheliocytes. In comparison with GOX, MDA induced more pronounced changes in physical and chemical properties of LDL particles. On the other hand, GOX-modified LDL particles were more prone to oxidation and aggregation than MDA-modified LDL. Incubation of endotheliocytes with MDA increased cell mechanical stiffness in contrast to incubation with GOX, which decreased it. [ABSTRACT FROM AUTHOR]

The aim of the present work was to identify structural, spatial, and quantitative changes in elements of the paranigral nucleus (PNN) of the midbrain and anterior cingulate field (ACF) of the telencephalon in different conditions of circulatory hypoxia. The anterior medial part of the PNN and layers V-VI of the ACF were studied in healthy rats seven days ( n = 4) after occlusion of both common carotid arteries and in intact (control 1, n = 4) and sham-operated (control 2, n = 4) rats. Histological sections stained with cresyl violet by the Nissl method and processed for detection of glial fibrillary acidic protein and Iba1 protein were used to identify the ratio of essentially unchanged, hypochromic, pyknomorphic, and ghost neurons, along with the numbers of astrocytes, oligodendrocytes, microgliocytes, and endotheliocytes. The areas of neurons and gliocyte bodies were measured, along with the distances from these cells to capillary walls, and gliocyte:neuron indexes were calculated. The results showed that after exposure to different conditions of circulatory hypoxia, the cellular elements of the brain showed a spectrum of characteristic pathological changes. Neurons showed signs of nuclear pyknosis, lysis, and conversion to 'ghost' cells. Cells in the nuclear zone of hypoxia tended to undergo death or pyknosis. Neurons located outside the hypoxic area and exposed only to the humoral actions of the responses of the glutamate-calcium cascade often showed acute swelling. The reactions of microgliocytes, with minor increases in numbers and structural signs of activation, represented early diffuse signs of focal hypoxia in the forebrain. Endotheliocyte proliferation seen at seven days of ischemia was not associated with the chain of cascade reactions, but occurred only in the focus of hypoxia. The concentrations of viable neurons and astrocytes close to blood capillaries and the increase in the number of satellite types of glial cells represent an adaptive mechanism and a constitute a condition for cell survival in the conditions of various types of cerebral ischemia. [ABSTRACT FROM AUTHOR]

Primary cell cultures derived from human myocardial explants were obtained and characterized. The explant cultures contained cardiac stem cells (c-kit +; ~4%), microvascular cells (endothelial cells and pericytes), fibroblasts, and myofibroblasts. It was demonstrated that culturing of cardiac cells in cardiospheres did not promote enrichment of the cell culture with stem cells. MACS-sorted c-kit + cells from the explant culture were characterized by limited proliferative capacity and were capable of cardiomyogenic differentiation. The presence of microvascular cells determined general angiogenic potential of the culture. [ABSTRACT FROM AUTHOR]

Long-term vibration exposure of humans leads to development of manifest atrophy and structural mosaicism of the bronchial epithelium in the mucosa of the large bronchi (diffuse degeneration of multilamellar cylindrical epithelium, focal hyperplasia, and squamous cell metaplasia). The mucosal subepithelial stroma is characterized by sclerosis, hypoelastosis, and reduction of microvessels. Radioautography confi rms the reduction of protein-producing activity of bronchial epitheliocytes and endotheliocytes. [ABSTRACT FROM AUTHOR]

The lung vessels of male C57Bl/6 mice were studied by immunohistochemical and stereometric methods on days 1, 3, 6, and 10 after intranasal infection with influenza A/H5N1 A/Goose/Krasnoozerskoye/627/05 virus. Influenza virus replicates in mouse lung vascular endotheliocytes and persists in these cells until the beginning of convalescence (day 10 after infection). This indicates high pathogenic activity of this strain. Active proliferation and apoptosis of endotheliocytes are detected early after infection; the counts of endotheliocytes expressing lysosomal hydrolases and NO-synthases increase many-fold. [ABSTRACT FROM AUTHOR]

Results of injection of autologous bone marrow mesenchymal stem cells with transfected GFP gene into the rat uterine horn cicatrix were studied by light microscopy. Large groups of blood vessels with blood cells inside were seen after injection of autologous bone marrow cells into the cicatrix on the right horn, formed 2 months after its ligation; no groups of vessels of this kind were found in the cicatrix in the contralateral horn. Examination of unstained sections in reflected UV light showed sufficiently bright fl uorescence in the endothelium and outer vascular membrane in the uterine horn cicatrix only on the side of injection. Hence, autologous mesenchymal stem cells injected into the cicatrix formed the blood vessels due to differentiation into endotheliocytes and pericytes. The expression of GFP gene not only in the vascular endothelium, but also in vascular outer membranes indicated that autologous mesenchymal stem cells differentiated in the endothelial and pericytic directions. [ABSTRACT FROM AUTHOR]

Experiments were performed on Wistar rats divided into three groups: group 1 (experimental group) consisted of rats subjected to hypoxia and treated with Salifen (15 mg/kg for 14 days); group 2 (controls) consisted of rats subjected to hypoxia but not treated; group 3 consisted of intact animals (each group included 8-10 animals). Light and electron microscopy methods were used to study the effects of Salifen on the structural characteristics of elements of the blood-brain barrier (BBB) of the neocortex in rats after exposure to hypoxia during the early postnatal period - on day 2 of life (a model of premature birth in humans). The results showed that Salifen had positive actions on the state of the microcirculatory bed after perinatal hypoxia, particularly in relation to state of endotheliocytes. Salifen was found to take active part in compensatory-adaptive reactions of the BBB in response to hypoxia; these experiments identified potential for further studies of the protective properties of Salifen. [ABSTRACT FROM AUTHOR]

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]

Using differential G-staining of chromosomes, the karyotype of the endothelial cell line ECV304 obtained from endotheliocytes of the human umbilical vein was studied. The cells have been shown to have a polyploid karyotype with a number of chromosomes ranging from 96 to 112, as well as multiple numerical and structural clonal chromosome abnormalities. The structural rearrangements involve almost all chromosomes of the karyotype. Several paired chromosomal rearrangements have been revealed and include del(9)(p21), as well as two derivates of chromosome 3 with a breakpoint at the p25 locus, i.e., der(3)t(3;12)(3p25;12q11∼12;12q21∼24.?1) and der(3)t(3;?)(3p25). The role of these rearrangements in the immortalization of endotheliocytes and in angiogenesis is discussed. A comparison of the karyotypes of the cell line ECV304 and of the bladder carcinoma T24 cell line has shown that these karyotypes differ in all of the main cytogenetic characteristics. No identical structural chromosomal rearrangements, nor rearrangements characteristic of bladder carcinoma cells have been revealed. The studied endothelial cell line ECV304 is not identical to the T24 cell line. [ABSTRACT FROM AUTHOR]

Stromal stem cells from human dental pulp (SBP-DPSCs) were used to study osteogenic differentiation in vitro and in vivo. We previously reported that SBP-DPSCs are multipotent stem cells able to differentiate into osteoblasts, which synthesize three-dimensional woven bone tissue chips in vitro. In this study, we followed the temporal expression pattern of specific markers in SBP-DPSCs and found that, when differentiating into osteoblasts, they express, besides osteocalcin, also flk-1 (VEGF-R2). In addition, 30% of them expressed specific antigens for endothelial cells, including CD54, von-Willebrand (domain 1 and 2), CD31 (PECAM-1) and angiotensin-converting enzyme. Interestingly, we found endotheliocytes forming vessel walls, observing that stem cells synergically differentiate into osteoblasts and endotheliocytes, and that flk-1 exerts a pivotal role in coupling osteoblast and endotheliocyte differentiation. When either SBP-DPSCs or bone chips obtained in vitro were transplanted into immunocompromised rats, they generated a tissue structure with an integral blood supply similar to that of human adult bone; in fact, a large number of HLA-1+ vessels were observed either within the bone or surrounding it in a periosteal layer. This study provides direct evidence to suggest that osteogenesis and angiogenesis mediated by human SBP-DPSCs may be regulated by distinct mechanisms, leading to the organization of adult bone tissue after stem cell transplantion.Cell Death and Differentiation (2007) 14, 1162–1171. doi:10.1038/sj.cdd.4402121; published online 9 March 2007 [ABSTRACT FROM AUTHOR]

Experiments on smooth muscle strips isolated from the capsule of bovine mesenteric lymph node showed that heparin low concentrations (0.010-0.025 U/ml) stimulating spontaneous isometric phasic contractions of smooth muscles, but higher heparin concentrations reduced or even completely eliminated these contractions. The inhibitory effects of heparin were presumably realized via stimulation of NO production by endothelial cells of the subcapsular space followed by activation of ATP-sensitive potassium channels of capsular myocytes and via modulation of prostaglandin synthesis. [ABSTRACT FROM AUTHOR]

Combined hepatitis C and B virus infection is associated with phenotypic heterogeneity of hepatocyte populations. Patchy distribution of hepatocyte ultrastructural changes is due to the diversity of complex cytopathic effects of these viruses. RNA-containing hepatitis C virus impairs mainly the cytoplasmic compartment of liver parenchymal cells and does not affect the nucleus. DNA-containing hepatitis B virus induces degradation of the nuclear compartment. [ABSTRACT FROM AUTHOR]

The cytotoxic effect of low-density lipoproteins on cultured human umbilical vein endothelial cells increases with their concentration, degree of oxidation, and incubation time, being more pronounced in ischemia or ischemia+reperfusion than in aerobic conditions. Synergism of the cytotoxic effect of lipoproteins with the damaging effect of ischemia and reperfusion promotes the development of atherosclerotic lesions of the vascular wall at sites predisposed to the damage by the ischemia/reperfusion. [ABSTRACT FROM AUTHOR]

Reorganization of sinusoidal cells (endotheliocytes, Kupffer cells, and Ito cells) in the liver microregion of male rat liver exposed to 3,4-benzopyrene was studied. Synchronous activation of the lysosome-vacuole systems in Kupffer cells and endotheliocyte indicates cooperation of these cells in detoxification of benzopyrene and its metabolites. Ito cells lose lipid inclusions and actively proliferate; the appearance of intermediate forms between lipocytes and fibroblasts attests to activation of fibrogenesis in the liver. [ABSTRACT FROM AUTHOR]