Разработка автоматизированной системы управления блока подготовки газа факельного сепаратора

Объектом исследования является блок подготовки газа (сепаратор факельной системы) установки комплексной подготовки газа. Цель работы – разработка автоматизированной системы управления сепаратора факельной системы УКПГ с использованием ПЛК, на основе выбранной SCADA-системы. В данном проекте была разработана система контроля и управления технологическим процессом на базе промышленных контроллеров Siemens, с применением SCADA-системы CodeSys.The object of the study is the gas treatment unit (the separator of the flare system) of the complex gas treatment unit. The purpose of the work is to develop an automated control system of the separator of the flare system of the UCP using PLC, based on the selected SCADA – system. This project was a developed system of control and management of technological process on the basis of industrial controllers of Siemens, with the use of SCADA-system CodeSys

Morphological characterization of liver fibrogenesis in animal models with genetically modulated TGF-beta signal transduction

Production of fibrous scar tissue in the liver is a normal response to injuries. In fibrosis this healing process is disturbed. Liver fibrosis is defined as the accumulation this fibrous scar tissue in the liver. After hepatocyte damage due to e.g. viral infection, heavy alcohol consumption, toxins or trauma, the immune system is activated and the cell repair process of the liver is induced. Injury or death (necrosis) of hepatocytes further stimulates inflammatory immune cells to release cytokines, growth factors, like TGF-beta activating hepatic stellate cells (HSCs) to produce collagen, glycoproteins (such as fibronectin) and proteoglycans. Activatied HSCs differentiate into myofibroblasts expressing alpha-smooth muscle actin (alpha SMA) which are deposited in the liver to form the extracellular matrix (ECM). At the same time, the process of breaking down or degrading collagen is impaired. In a healthy liver, synthesis (fibrogenesis) and degradation (fibrolysis) of matrix tissue are in balance. Fibrosis occurs when scar tissue is generated in excess and faster than it is degraded and removed from the liver. TGF-beta is known to play a central role in regulation of the production, degradation, and accumulation of ECM proteins and that, as a consequence, it may play a pivotal role in the fibroproliferative changes that follow tissue damage in many vital organs, including liver, lung, kidney, skin, heart, and arterial wall.(Massague, J. 1990). Therefore numerous antifibrotic strategies aim to block action of this cytokine or reduce its synthesis. TGF-beta superfamily members bind to serine/threonine kinase receptors. expressing on surface of a variety of cells e.g. hepatocytes and HSCs. TGF-beta receptors comprise two structurally similar subfamilies, the type I and type II receptors, both with small cysteine rich extracellular regions and intracellular portions consisting mainly of their kinase domains. To transmit a signal, type II and type I receptors act in sequence (Wrana et al., 1994). TGF-beta first binds to T beta RII, which resides in the cell membrane in an oligomeric form with intrinsic kinase activity; T beta RI is then recruited and phosphorylated in its GS domain by T beta RII, leading to activation of its kinase activity and subsequent intracellular signaling (Massague 1998 and Piek et al.,1999). Smad7 belongs to inhibitory Smad propteins.(I-Smad) exerting their inhibitory effect on TGF-beta by binding to the T beta RI to hinder posphorylation of Smad2 (receptor Smad, R-Smad) and subsequent signaltransduction pathway to nucleus. Because the expression of Smad7 is upregulated by TGF-beta, this molecule is an important feedback inhibitor of TGF-beta signaling (Dooley et al., 2003). Since Smad7 represents an efficient inhibitor of TGF-beta signaling, it is conceivable that hyperexpression of Smad7 is an additional means to antagonize TGF-beta in fibrogenesis. In a part of my own work, we studied the effect of Smad7 overexpression after adenoviral gene transfer (AdSmad7) in primary cultured HSCs and in vivo after BDL of rats (Dooley et al., 2003). Exogenous Smad7 overexpression prevented BDL dependent activation of HSCs and liver fibrosis. Collagen I deposition and hydroxyproline content were significantly reduced in Smad7 overexpressing livers.. As AdSmad7 viruses infected and resided in all cell types of the liver, specificity of its effect could not be related to a single cell type. Even an influence on other organs could not be excluded. In my thesis I therefore established an animal model with inducible overexpression of transgenic Smad7 in hepatocytes (S7tg mice) and studied its effect on fibrogenesis after CCl4 induced liver damage. In contrast to albumin/TGF-beta 1 transgenic mice of Sanderson and colleagues (Sanderson et al., 1995) the mortality rate of S7tg mice was infinitely small during the CCl4 treatment protocol I used. In S7tg mice the Smad7 gene was expressed under the control of the human CRP promoter. CRP is a component of the congenital immune system stimulated by LPS. Binding of LPS to cell surface receptors triggers the synthesis of inflammatory cytokines including IL-6, which then induces expression of CRP (Agrawal et al., 2001). Because CRP and its transcription factors are mainly expressed in hepatocytes, this new mouse model leads to specific Smad7 expression in hepatocytes. These mice and corresponding controls were treated with CCl4 for 8 weeks. In addition, mice with a disrupted Smad7 gene (S7 Delta E1) were investigated. The S7 Delta E1 strain displayed the highest degree of fibrosis, indicating that the presence of a functional negative feedback regulation for TGF-beta signaling is controling the degree of fibrogenesis. Interestingly, Smad7 overexpression in hepatocytes of CRP-Smad7 transgenic mice was sufficient to reduce fibrosis and expression of protein markers in the liver, e.g., collagen and alpha-SMA, as well as in serum, e.g., aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP) and hyaluronic acid (HA), by more than 70% in comparison to wild type animals. Further, Smad7 overexpression reduces proliferation, inflammation and apoptotic processes in liver cells of CRP-Smad7 transgenic mice. Taken together, my thesis demonstrates that TGF-beta signaling in hepatocytes is required for progression of chronic liver disease and blocking its signaling pathway in this cell type by ectopic expression of Smad7 is sufficient to obtain a beneficial outcome

Morphological characterization of liver fibrogenesis in animal models with genetically modulated TGF-beta signal transduction

Production of fibrous scar tissue in the liver is a normal response to injuries. In fibrosis this healing process is disturbed. Liver fibrosis is defined as the accumulation this fibrous scar tissue in the liver. After hepatocyte damage due to e.g. viral infection, heavy alcohol consumption, toxins or trauma, the immune system is activated and the cell repair process of the liver is induced. Injury or death (necrosis) of hepatocytes further stimulates inflammatory immune cells to release cytokines, growth factors, like TGF-beta activating hepatic stellate cells (HSCs) to produce collagen, glycoproteins (such as fibronectin) and proteoglycans. Activatied HSCs differentiate into myofibroblasts expressing alpha-smooth muscle actin (alpha SMA) which are deposited in the liver to form the extracellular matrix (ECM). At the same time, the process of breaking down or degrading collagen is impaired. In a healthy liver, synthesis (fibrogenesis) and degradation (fibrolysis) of matrix tissue are in balance. Fibrosis occurs when scar tissue is generated in excess and faster than it is degraded and removed from the liver. TGF-beta is known to play a central role in regulation of the production, degradation, and accumulation of ECM proteins and that, as a consequence, it may play a pivotal role in the fibroproliferative changes that follow tissue damage in many vital organs, including liver, lung, kidney, skin, heart, and arterial wall.(Massague, J. 1990). Therefore numerous antifibrotic strategies aim to block action of this cytokine or reduce its synthesis. TGF-beta superfamily members bind to serine/threonine kinase receptors. expressing on surface of a variety of cells e.g. hepatocytes and HSCs. TGF-beta receptors comprise two structurally similar subfamilies, the type I and type II receptors, both with small cysteine rich extracellular regions and intracellular portions consisting mainly of their kinase domains. To transmit a signal, type II and type I receptors act in sequence (Wrana et al., 1994). TGF-beta first binds to T beta RII, which resides in the cell membrane in an oligomeric form with intrinsic kinase activity; T beta RI is then recruited and phosphorylated in its GS domain by T beta RII, leading to activation of its kinase activity and subsequent intracellular signaling (Massague 1998 and Piek et al.,1999). Smad7 belongs to inhibitory Smad propteins.(I-Smad) exerting their inhibitory effect on TGF-beta by binding to the T beta RI to hinder posphorylation of Smad2 (receptor Smad, R-Smad) and subsequent signaltransduction pathway to nucleus. Because the expression of Smad7 is upregulated by TGF-beta, this molecule is an important feedback inhibitor of TGF-beta signaling (Dooley et al., 2003). Since Smad7 represents an efficient inhibitor of TGF-beta signaling, it is conceivable that hyperexpression of Smad7 is an additional means to antagonize TGF-beta in fibrogenesis. In a part of my own work, we studied the effect of Smad7 overexpression after adenoviral gene transfer (AdSmad7) in primary cultured HSCs and in vivo after BDL of rats (Dooley et al., 2003). Exogenous Smad7 overexpression prevented BDL dependent activation of HSCs and liver fibrosis. Collagen I deposition and hydroxyproline content were significantly reduced in Smad7 overexpressing livers.. As AdSmad7 viruses infected and resided in all cell types of the liver, specificity of its effect could not be related to a single cell type. Even an influence on other organs could not be excluded. In my thesis I therefore established an animal model with inducible overexpression of transgenic Smad7 in hepatocytes (S7tg mice) and studied its effect on fibrogenesis after CCl4 induced liver damage. In contrast to albumin/TGF-beta 1 transgenic mice of Sanderson and colleagues (Sanderson et al., 1995) the mortality rate of S7tg mice was infinitely small during the CCl4 treatment protocol I used. In S7tg mice the Smad7 gene was expressed under the control of the human CRP promoter. CRP is a component of the congenital immune system stimulated by LPS. Binding of LPS to cell surface receptors triggers the synthesis of inflammatory cytokines including IL-6, which then induces expression of CRP (Agrawal et al., 2001). Because CRP and its transcription factors are mainly expressed in hepatocytes, this new mouse model leads to specific Smad7 expression in hepatocytes. These mice and corresponding controls were treated with CCl4 for 8 weeks. In addition, mice with a disrupted Smad7 gene (S7 Delta E1) were investigated. The S7 Delta E1 strain displayed the highest degree of fibrosis, indicating that the presence of a functional negative feedback regulation for TGF-beta signaling is controling the degree of fibrogenesis. Interestingly, Smad7 overexpression in hepatocytes of CRP-Smad7 transgenic mice was sufficient to reduce fibrosis and expression of protein markers in the liver, e.g., collagen and alpha-SMA, as well as in serum, e.g., aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP) and hyaluronic acid (HA), by more than 70% in comparison to wild type animals. Further, Smad7 overexpression reduces proliferation, inflammation and apoptotic processes in liver cells of CRP-Smad7 transgenic mice. Taken together, my thesis demonstrates that TGF-beta signaling in hepatocytes is required for progression of chronic liver disease and blocking its signaling pathway in this cell type by ectopic expression of Smad7 is sufficient to obtain a beneficial outcome

Tenth and Twelfth Nerve Palsies in a Patient with Internal Carotid Artery Dissection Mistaken for Cervical Mass Lesion

Among the multiple causes for cranial nerve palsies, internal carotid artery dissection is rather uncommon. Patients usually present with unilateral head pain, Horner's syndrome, and signs of cerebral ischemia. We present the case of a 52-year-old male patient, who showed isolated palsies of the tenth and twelfth nerve without any other symptoms. Magnetic resonance imaging (T1) depicted a hyperintense lesion surrounding the internal carotid artery, which was mistaken for a cervical mass, and the patient underwent unnecessary surgical exploration of the neck. Angiography performed afterward could reveal the dissection of the internal carotid artery. This case shows that even in cases with mild and atypic symptoms, internal carotid artery dissection has always to be ruled out in lower cranial nerve palsies

Anti-phospholipase A2 receptor antibody in idiopathic membranous nephropathy: A report from Iranian population

Background: Idiopathic Membranous Nephropathy (iMN) is the most common cause of nephrotic syndrome in adults. Approximately one third of patients with iMN progress to end-stage renal disease. Anti-phospholipase A2-receptor (anti-PLA2R) antibodies are present in patients with iMN and appear to play a role in the pathogenesis of iMN. Objectives: In this study, we explored the prevalence of anti-PLA2R antibodies in a cohort of patients with iMN in Iran. We also sought to determine circulating levels of anti-secretory PLA2 (anti-sPLA2) antibodies in those with anti-PLA2R antibodies. Patients and Methods: Using an indirect immunofluorescence assay, we measured anti-PLA2R antibodies in a group of patients with iMN in Iran. The serum levels of anti-sPLA2 antibodies were also measured in those with positive results for anti-PLA2R antibodies. Results: We studied 23 patients with iMN (M/F 12/11, 34±9.8 year), two patients with secondary MN and five patients with the nephrotic syndrome of other causes.Anti-PLA2R antibodies were detected in 17/23 (74%) of patients with iMN, but not in those with secondary MN or other forms of primary glomerular diseases. We found no correlation between anti-PLA2R antibody titer and the degree of proteinuria. We found high titers of anti-sPLA2 antibodies in a subset of patients with high levels of anti-PLA2R antibodies. Conclusions: Anti-PLA2R antibodies are specific for iMN. Proteinuria may also reflect glomerular structural damage rather than immunological activity of the disease. The preliminary idea of any presumptive role of anti-sPLA2antibodies in iMN needs further investigation

За кадры. 1973. № 51 (1726)

Государственная забота о молодежиОшибки в выборе нет / О. МарченкоОгни факультета / Р. ЧернаяЗнания и только знания. За "круглым столом" - экзаменаторы / [беседа с] И. О. ДавыденкоОдна мечта / Г. ИгловскаяЗать и понимать сущность явлений. За "круглым столом" - экзаменаторы / [беседа с] Н. Л. ВишневскаяС думой об абитуриенте / О. СоловьеваВести с практики / [беседа с] В. Ф. Жидобин ; [беседа с] А. Н. Шайтаров ; [беседа с] П. А. Самойлов ; [беседа с] Г. М. Степнова ; [беседа с] О. Н. Мартыненко ; Д. К. АвдееваЖаркое лето "Севера" / С. КошиковаУмейте обобщать. За "круглым столом" - экзаменаторы / [беседа с] Е. С. НовиковаЛитература - предмет профилирующий. За "круглым столом" - экзаменаторы / [беседа с] А. И. СальникЛетит "Голубая стрела". Зачетка трудового семестра / Л. ПавловаОт грозы до грозы / Н. БлыщикСанитарная пятница / С. Кузнецо

Impact of surgeons' experience and the single-shot perioperative antibiotic prophylaxis on outcome in stapedotomy.

BackgroundThe aim of this study was to evaluate whether surgeons´ experience and perioperative single-shot antibiotic prophylaxis affect outcome of patients undergoing stapes surgery.Patients and methodsWe retrospectively evaluated audiological outcomes and postoperative complications of 538 consecutive patients who underwent stapes surgery at a single tertiary referral center between 1990 and 2017. Effects of different clinical variables, including single-shot antibiotic prophylaxis and surgeons' experience on outcome were assessed.Results538 patients underwent 667 stapedotomies and postoperative complication rate was 7.5% (n = 50). Air conduction and air-bone gap closure improved significantly after surgery (14.2 ± 14.8 dB, p = 0.001; 14.5 ± 12.8 dB, p = 0.001). Multivariate analysis revealed that 6 years or less of surgical experience was independently associated with a higher incidence of persisting or recurrent conductive hearing loss (p = 0.033, OR 5.13) but perioperative application of antibiotics had no significant effect on outcome.ConclusionFirst, clinical outcome regarding persisting or recurrent conductive hearing loss caused by incus necrosis and prosthesis luxation is linked to surgical performance. This underlines the need for a meticulous training and supervision of less experienced surgeons performing stapes surgery. Second, our results do not support the need for perioperative antibiotic prophylaxis in stapes surgery. Potential standard limitations of retrospective cohort studies (selection bias, confusion bias etc.) could play a role in interpreting our results. However, the probability for these limitations is minimized due to the large patient sample