28 research outputs found

    Peculiarities of synthesis of matrix metalloproteinase-9 in the lungs during experimental development of distress syndrome

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    Acute respiratory distress syndrome (ARDS) was reproduced in nonlinear male rats by intratracheal instillation of 45—55 thousand, lysate rat neutrophils (method patented in RF); the control group was injected with saline solution. The animals were taken from the experiment at 1, 3 and 6 days, the expression of matrix metallopro-teinase-9 (MMP-9) by cells of the lungs was determined, by immunohistochemistry at each days. The expression of MMP-9 was found in neutrophils, macrophages, fibroblasts, endothelium and. type 2 alveolocytes in the both groups. In the control group the expression, of MMP-9 was found equally low in the all cells, except type 2 alveolocytes. It was decreased in type 2 alveolocytes on day 6. A significant increase in the expression of MMP-9 was found in neutrophils, macrophages, fibroblasts endothelium and type 2 alveolocytes in the exudative stage of ARDS. In the proliferative stage the expression of MMP-9 was high in all the cells, decreasing only in type 2 alveolocytes. In the fibrotic stage of expression of MMP-9 returned to the level of the control group in macrophages, type 2 alveolocytes, the endothelium; in neutrophils and fibroblasts it remained high

    Dynamics of the chemokine ENA-78/CXCL5 levels in blood serum and skin exudate in patients with atopic dermatitis

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    Currently, there are only scarce data on dynamics of biologically active substances in the lesions associated with atopic dermatitis. Persistence of microorganisms in atopic dermatitis is high on the skin surface. However, pathophysiological significance of ENA-78/CXCL5 for development of atopic dermatitis was not studied so far. The ENA-78/CXCL5 is known to be produced by endotheliocytes, keratinocytes, eosinophils, fibroblasts to activate neutrophil migration, especially under the influence of LPS-containing microorganisms. The aim of this study was to evaluate the dynamics of ENA-78/CXCL5 chemokine levels in blood serum and skin exudates in the patients with atopic dermatitis, as well as to determine pathophysiological role of the chemokine in pathogenesis of dermatosis. 80 patients with limited and widespread forms of atopic dermatitis and 15 volunteers were under observation. The dynamics of ENA-78/CXCL5 levels was studied in blood sera and skin exudates. Blood samples for the study were drawn at the time periods of exacerbation and remission. Skin exudates were taken from the patients during the exacerbation period using disposable insulin syringes and 20-G disposable needles. In healthy volunteers, the skin exudate was obtained by the “skin window” technique as described by V.V. Klimov and coauthors “A method for assessing minimal inflammatory activity of skin in atopic dermatitis in remission”. The cell analysis was conducted by flow cytofluorimetry using the LEGEND plex TM Human Proinflammatory Chemokine Panel (USA) according to the manufacturer’s protocol. Serum concentrations of chemokine ENA-78/CXCL5 in adolescents with atopic dermatitis, exceeded the range for healthy volunteers. During remission of dermatitis, the chemokine level did not reach the indices in the control group. In adults, the ENA-78/CXCL5 concentration, both at the onset of symptoms and upon their resolution, was below the control levels. Maximal concentrations of ENA-78/CXCL5 chemokine were detected in the skin exudates. As based on our data on the dynamics of ENA-78/CXCL5 chemokine levels, it could be assumed that this substance may represent a sufficient link in pathogenesis of atopic dermatitis, by causing migration of neutrophils and monocytes to the affected area. The ENA-78/CXCL5 chemokine may be a marker of microbial pathogenesis and cellular damage in atopic dermatitis

    PROGNOSTIC FACTORS OF OUTCOMES OF TREATMENT OF ACUTE NONSPECIFIC EMPIEMA PLEURAE

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    The purpose of the given work is specification adverse prognostical criteria of outcomes of treatment of acute nonspecific empiema pleurae. Work is based on the results of complex treatment of 123 patients with empiema pleurae of not traumatic character. The acute abscess and a lung gangrene (37,9 %) was a principal cause of development of empiema. It is established that the most authentic factors of failures of treatment of empiema were overdue diagnostics acute empiema pleurae; defects and errors in treatment; insufficient preoperative preparation of the patient; an insufficient skill level of the surgeon; late reference for medical aid. Preventive maintenance of the specified defects of rendering of medical aid for the patient with acute empiema pleurae will allow to improve results of treatment of patients with the given pathology

    The role of HSP-70 in the pathogenesis of respiratory distress syndrome induced by influenza pneumonia

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    Lung paraffin sections of 35 died during the epidemic of influenza A/H1N1 of 2009-2010 in Zabaikalskiy krai were investigated. Exudative stage was diagnosed, in 10 cases, proliferative stage - in 16 cases and fibrotic stage of acute respiratory distress syndrome (ARDS) was diagnosed in 9 cases at the autopsy. Expression of heat shock protein 70 (HSP-70) by cells of the lungs was determined in sections by immunohistochemistry. We revealed that HSP-70 is expressed by neutrophils, macrophages, fibroblasts and alveolocytes type 1 and. 2. It was found that regardless of the stage of ARDS the highest expression of HSP-70 was realized by neutrophils, the lowest - by the endothelium alveolocytes type 2 and. fibroblasts. HSP-70 expression in neutrophils, macrophages, fibroblasts and. alveolocytes type 1 was the same in all stages of ARDS. In alveolocytes type 2 in exudative and. proliferative phases it was lower than at the development of fibrosis. We concluded that one of the mechanisms of developments of acute lungs injury/acute respiratory distress syndrome at influenza pneumonia is comparatively low synthesis of HSP-70 by endotheliocytes of lung capillary and. alveolocytes type 2

    Pathophysiological role of chemokine MIG/CXCL9 in the development of atopic dermatitis

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    Background. In patients with atopic dermatitis, the persistence of microorganisms on the skin surface is high, which can enhance the expression of MIG/CXCL9, exacerbating inflammation and activating keratinocyte apoptosis, however, the dynamics of this chemokine in atopic dermatitis has not been studied.The aim. To study the concentration of chemokine MIG/CXCL9 in the dynamics of atopic dermatitis and determine its role in the pathogenesis of dermatosis.Materials and methods. The study included 80 patients aged 13 to 44 years with limited and widespread atopic dermatitis and 30 practically healthy volunteers. The therapy of patients, the collection of biological material were carried out in the Regional Dermatovenerologic Dispensary in Chita, laboratory tests were performed at the Chita State Medical Academy in the period from 2018 to 2020. The MIG/CXCL9 level was studied during exacerbation and remission of the disease in blood serum and skin exudate by flow cytofluorimetry using LEGENDplex Human Proinflammatory Chemokine Panel (BioLegend, USA). In healthy volunteers, skin exudate sampling was carried out by the “skin window” method. For statistical processing, the Microsoft Excel (Microsoft Corp., USA) application software package and SPSS Statistics 25.0 (IBM Corp., USA) were used.Results. The concentration of chemokine MIG/CXCL9 in the skin exudate is greater than in the blood serum. With a limited form of the disease in adolescents, the level of MIG/CXCL9 in the skin exudate is 8.1 times higher than the control values, with a common form – 9.3 times. In adults with advanced atopic dermatitis, the concentration of chemokine IL/CXCL9 in the skin exudate is 20.8 times higher than the values of the control group.Conclusion. In atopic dermatitis, the level of chemokine MIG/CXCL9 is higher in the cutaneous pathological process. In the pathogenesis of the disease, MIG/ CXCL9 inhibits collagen synthesis and promotes apoptosis of keratinocytes, followed by the formation of hyperreactivity of the skin, its dryness and peeling

    Time course of autoantibodies to collagen type I and III in blood serum and skin exudate in atopic dermatitis

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    In accordance with Clinical Guidelines of the Russian Society of Dermatovenerologists and Cosmetologists, atopic dermatitis is a chronic allergic genetically determined dermatosis of a multifactorial nature. There are, however, some aspects that challenge the allergic nature of dermatosis. For example, according to literature data, not all the patients have increased synthesis of immunoglobulin E, some of them are torpid to antihistamine treatment, and, when examining the skin of some patients with atopic dermatitis, an absolute polymorphism of rashes is revealed, thus being not typical to the reagin-type allergic reactions. According to modern data, autoimmune theory is assumed for the mechanisms of atopic dermatitis. However, objective proofs of this theory have not been presented, thus drawing our attention to the studies of this issue. The aim of this study was to identify autoimmune pathogenetic mechanisms of atopic dermatitis. The study included 40 adolescents and 40 adult patients with limited and extended forms of atopic dermatitis. The patients were evaluated during the period of exacerbation and remission of the disease. Blood and skin exudates samples were taken from all the patients. The control group consisted of 30 practically healthy volunteers in whom skin exudate was obtained by the “skin window” technique as proposed by Klimov V.V. et al. “A method for assessing minimal inflammatory activity of skin in atopic dermatitis in remission”. Concentrations of IgG autoantibodies to collagen types I and III were determined in blood serum and skin exudate samples applying ELISA techniques with ready-made panels AEA571Hu ELISA Kit for Anti-Collagen Type I Antibody (USA), AEA176Hu ELISA Kit for Anti-Collagen Type III Antibody (USA), according to the manufacturer’s protocols. For the first time, the contents of autoantibodies to skin collagen types I and III in the patients with atopic dermatitis we studied in parallel, i.e., at systemic level and in affected skin. If compared to the group of healthy volunteers, the concentration of autoantibodies to collagen types I and III was found to be increased in all the patients with atopic dermatitis, both during exacerbation and in remission of the disease. The maximal values of autoantibodies to collagen types I and III were recorded in blood serum upon development of clinical symptoms of dermatosis, along with low contents of these antibodies detectable in their skin exudates. Permanently high concentrations of autoantibodies to collagen types I and III in blood serum at exacerbation and remission of atopic dermatitis, and their low level in their skin exudate suggest emergence of circulating and precipitating immune complexes, thus allowing us to consider atopic dermatitis as an autoimmune process

    Functional activity of the oral endothelium in persons, with chronic periodontitis during treatment with plasmolifting

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    Chronic periodontitis as an osteoimmune disease of the oral cavity is accompanied by a change in the functional activity of endotheliocytes. Moreover, abnormal vascularization exacerbates periodontal inflammation, as it promotes the transmigration of a larger number of immunocompetent cells, the influx of inflammatory mediators and cytokines.The aim of our work was to study the functional activity of the endothelium of the vessels of the oral cavity in persons suffering from chronic periodontitis in the treatment of plasmolifting.Materials and methods. Under observation were 30 patients diagnosed with chronic generalized periodontitis of moderate severity at the age of 35 (32.50; 40.00) years, with no severe somatic pathology (main group). The comparison group included 20 people aged 38 (34.00; 45.00) years with no inflammatory diseases in the oral cavity. All patients underwent local anti-inflammatory therapy and sanitation of periodontal pockets, correction of occlusal contacts, curettage, plasma lifting. Oral fluid concentration of soluble adhesion molecules ICAM-1 and VCAM-1, endothelin-1, qualitative and quantitative composition of microflora were determined.Results. After the treatment with plasmolifting, a noticeable relief of the activity of the inflammatory process was observed. In patients with chronic periodontitis, Porphyromonas gingivalis was found in 100 % of cases in a titer of 5.73 (4.9; 6.7) lg (gEq/sample), in 62.5 % – Prevotella intermedia in a titer of 4.5 (3.0; 5.5) lg (gEq/sample). Against the background of therapy, decrease of the occurrence of the microorganism and of the number of microorganisms was observed. The concentration of the soluble form of VCAM-1 in the oral fluid of patients with chronic periodontitis exceeded the values of the control group by 38.3 times (p = 0.000001), and ICAM-1 – by 18.1 times (p = 0.00001). Against the background of plasmolifting therapy, the level of the studied substances decreased, but exceeded the control values by 25.2 and 6.4 times, respectively. The content of endothelin in the oral fluid in patients with periodontitis exceeded the values of healthy individuals by 40.7 % (p = 0.003), during therapy its values decreased, but did not reach the level of healthy volunteers (p = 0.04)

    IMPROVEMENT OF METHODS OF REHABILITATION OF THE ABDOMINAL CAVITY WITH DIFFUSE PURULENT PERITONITIS UNDER EXPERIMENTAL CONDITIONS

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    This paper presents the results of experimental studies of intraoperative sanation of abdominal cavity at diffuse purulent peritonitis (in 25 dogs), compared with the results of readjustment of the abdominal cavity with diffuse purulent peritonitis (74 patients) using the universal domestic antiseptic "anolyte". The results of experimental and clinical studies show that presented method of readjustment of the abdominal cavity can be used in clinical practice

    Особенности экспрессии дефензинов в легких при остром респираторном дистресс–синдроме на фоне гриппозной пневмонии

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    Summary. We investigated paraffin slices of the lungs from 35 people died during the 2009 epidemic of influenza A / H1N1. The exudative stage of acute respiratory distress syndrome (ARDS) was diagnosed in 10 cases, the proliferative stage in 16 and the fibrotic stage in 9 cases. Expression of α–defensins (HNP 1–3) in lung tissue was determined by the immunohistochemistry. The highest HNP 1–3 expression level was found during the exudative stage in neutrophils; it was similar in macrophages and alveolocytes type 2. α–defensins were also expressed by the epithelium of terminal bronchioles. During the proliferative stage, the HNP 1–3 expression in neutrophils remained at the high level, it was increased in alveolocytes type 2 and was unchanged in macrophages. During this stage, HNP 1–3 additionally expressed by immature alveolocytes and squamous metaplasia epithelial cells in the terminal bronchioles. During the fibrotic stage, the HNP 1–3 expression in neutrophils was reduced but remained the highest in comparison with that in the other cells; it did not changed in the alveolocytes type 2 and the macrophages. In this stage, HNP 1–3 also expressed in proliferating fibroblasts
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