Corporate events

Сorporate events are an effective way for companies to engage with customers or employees. Any business that wants to build lasting relationships holds affairs of this kind. Hosting a corporate affair allows to enhance bonds with current clients and partners, and attract future ones

JNK activation is responsible for mucus overproduction in smoke inhalation injury

<p>Abstract</p> <p>Background</p> <p>Increased mucus secretion is one of the important characteristics of the response to smoke inhalation injuries. We hypothesized that gel-forming mucins may contribute to the increased mucus production in a smoke inhalation injury. We investigated the role of c-Jun N-terminal kinase (JNK) in modulating smoke-induced mucus secretion.</p> <p>Methods</p> <p>We intubated mice and exposed them to smoke from burning cotton for 15 min. Their lungs were then isolated 4 and 24 h after inhalation injury. Three groups of mice were subjected to the smoke inhalation injury: (1) wild-type (WT) mice, (2) mice lacking JNK1 (JNK1-/- mice), and (3) WT mice administered a JNK inhibitor. The JNK inhibitor (SP-600125) was injected into the mice 1 h after injury.</p> <p>Results</p> <p>Smoke exposure caused an increase in the production of mucus in the airway epithelium of the mice along with an increase in MUC5AC gene and protein expression, while the expression of MUC5B was not increased compared with control. We found increased MUC5AC protein expression in the airway epithelium of the WT mice groups both 4 and 24 h after smoke inhalation injury. However, overproduction of mucus and increased MUC5AC protein expression induced by smoke inhalation was suppressed in the JNK inhibitor-treated mice and the JNK1 knockout mice. Smoke exposure did not alter the expression of MUC1 and MUC4 proteins in all 3 groups compared with control.</p> <p>Conclusion</p> <p>An increase in epithelial MUC5AC protein expression is associated with the overproduction of mucus in smoke inhalation injury, and that its expression is related on JNK1 signaling.</p

Left Ventricular Diastolic Dysfunction Screening by a Smartphone-Case Based on Single Lead ECG.

Aims To investigate the potential of a signal processed by smartphone-case based on single lead electrocardiogram (ECG) for left ventricular diastolic dysfunction (LVDD) determination as a screening method. Methods and Results We included 446 subjects for sample learning and 259 patients for sample test aged 39 to 74 years for testing with 2D-echocardiography, tissue Doppler imaging and ECG using a smartphone-case based single lead ECG monitor for the assessment of LVDD. Spectral analysis of ECG signals (spECG) has been used in combination with advanced signal processing and artificial intelligence methods. Wavelengths slope, time intervals between waves, amplitudes at different points of the ECG complexes, energy of the ECG signal and asymmetry indices were analyzed. The QTc interval indicated significant diastolic dysfunction with a sensitivity of 78% and a specificity of 65%, a Tpeak parameter >590 ms with 63% and 58%, a T value off >695 ms with 63% and 74%, and QRSfi > 674 ms with 74% and 57%, respectively. A combination of the threshold values from all 4 parameters increased sensitivity to 86% and specificity to 70%, respectively (OR 11.7 [2.7-50.9], P < .001). Algorithm approbation have shown: Sensitivity-95.6%, Specificity-97.7%, Diagnostic accuracy-96.5% and Repeatability-98.8%. Conclusion Our results indicate a great potential of a smartphone-case based on single lead ECG as novel screening tool for LVDD if spECG is used in combination with advanced signal processing and machine learning technologies

High-molecular-weight hyaluronan – a possible new treatment for sepsis-induced lung injury: a preclinical study in mechanically ventilated rats

Introduction: Mechanical ventilation with even moderate-sized tidal volumes synergistically increases lung injury in sepsis and has been associated with proinflammatory low-molecular-weight hyaluronan production. High-molecular-weight hyaluronan (HMW HA), in contrast, has been found to be anti-inflammatory. We hypothesized that HMW HA would inhibit lung injury associated with sepsis and mechanical ventilation. Methods: Sprague–Dawley rats were randomly divided into four groups: nonventilated control rats; mechanical ventilation plus lipopolysaccharide (LPS) infusion as a model of sepsis; mechanical ventilation plus LPS with HMW HA (1,600 kDa) pretreatment; and mechanical ventilation plus LPS with low-molecular-weight hyaluronan (35 kDa) pretreatment. Rats were mechanically ventilated with low (7 ml/kg) tidal volumes. LPS (1 or 3 mg/kg) or normal saline was infused 1 hour prior to mechanical ventilation. Animals received HMW HA or low-molecular-weight hyaluronan via the intraperitoneal route 18 hours prior to the study or received HMW HA (0.025%, 0.05% or 0.1%) intravenously 1 hour after injection of LPS. After 4 hours of ventilation, animals were sacrificed and the lung neutrophil and monocyte infiltration, the cytokine production, and the lung pathology score were measured. Results: LPS induced lung neutrophil infiltration, macrophage inflammatory protein-2 and TNFα mRNA and protein, which were decreased in the presence of both 1,600 kDa and 35 kDa hyaluronan pretreatment. Only 1,600 kDa hyaluronan completely blocked both monocyte and neutrophil infiltration and decreased the lung injury. When infused intravenously 1 hour after LPS, 1,600 kDa hyaluronan inhibited lung neutrophil infiltration, macrophage inflammatory protein-2 mRNA expression and lung injury in a dose-dependent manner. The beneficial effects of hyaluronan were partially dependent on the positive charge of the compound. Conclusions: HMW HA may prove to be an effective treatment strategy for sepsis-induced lung injury with mechanical ventilation

Поражение сердца при AL-амилоидозе. Состояние проблемы

AL cardiac amyloidosis is a relatively rare disorder that belongs to the group of infiltrative cardiomyopathies. Diagnosis of primary amyloidosis is challenging due to many unspecific symptoms and sings, which often leads to late diagnosis when treatment options are limited. Primary amyloidosis particularly needs to be excluded in patients with heart failure with preserved ejection fraction. Therapy in cardiac amyloidosis has to main vectors: 1) chemotherapy to eliminate amyloidogenic plasmatic cells 2) heart failure treatment. The main challenge for cardiologists is to support hemodynamics until response to chemotherapy occurs. In the article the issue of diagnostics, risk stratification and treatment of primary cardiac amyloidosis is addressed.Актуальность. AL-амилоидоз сердца относится к группе инфильтративных кардиомиопатий и является относительно редким заболеванием. Диагностика амилоидоза сердца представляет большие трудности ввиду множества неспецифичных симптомов системного характера, что зачастую приводит к поздней постановке диагноза, когда варианты лечения довольно ограничены. Диагноз амилоидоза обязательно должен быть исключен у пациентов с сердечной недостаточностью с сохранной фракцией выброса. Лечение пациентов с амилоидозом сердца включает два основных направления ― проведение химиотерапии с целью уничтожения амилоидогенных плазматических клеток и лечение сердечной недостаточности. Основной задачей кардиолога является поддержание гемодинамики до получения ответа на химиотерапию. В статье рассматриваются вопросы диагностики, стратификации риска и лечения больных с первичным амилоидозом сердца. Заключение. Использование современной химиотерапии демонстрирует значительное улучшение выживаемости

Случай стрессиндуцированной кардиомиопатии

В последние годы в связи с широким применением ангиографии все чаще диагностируется кардиомиопатия (КМП) такотсубо (takotsubo), для которой характерны изменения ЭКГ, сходные с таковыми у больных с острым коронарным синдромом, повышение маркеров некроза сердечной мышцы и отсутствие значимого поражения КА. При вентрикулографии в типичных случаях выявляется транзиторное баллонирование верхушки левого желудочка. Патофизиологические механизмы, лежащие в основе этого заболевания, остаются до конца не выясненными, хотя многие исследователи относят его к редкой обратимой форме нейрогенной КМП. Авторами описан первый диагностированный ими случай КМП такотсубо, имеющий в целом типичные клинические и лабораторные проявления

Low-molecular-weight heparin reduces hyperoxia-augmented ventilator-induced lung injury via serine/threonine kinase-protein kinase B

<p>Abstract</p> <p>Background</p> <p>High-tidal-volume mechanical ventilation and hyperoxia used in patients with acute lung injury (ALI) can induce the release of cytokines, including high-mobility group box-1 (HMGB1), oxygen radicals, neutrophil infiltration, and the disruption of epithelial and endothelial barriers. Hyperoxia has been shown to increase ventilator-induced lung injury, but the mechanisms regulating interaction between high tidal volume and hyperoxia are unclear. We hypothesized that subcutaneous injections of enoxaparin would decrease the effects of hyperoxia on high-tidal-volume ventilation-induced HMGB1 production and neutrophil infiltration via the serine/threonine kinase/protein kinase B (Akt) pathway.</p> <p>Methods</p> <p>Male C57BL/6, either wild type or Akt^+/-, aged between 6 and 8 weeks, weighing between 20 and 25 g, were exposed to high-tidal-volume (30 ml/kg) mechanical ventilation with room air or hyperoxia for 2 to 8 hours with or without 4 mg/kg enoxaparin administration. Nonventilated mice served as a control group. Evan blue dye, lung wet-to-dry weight ratio, free radicals, myeloperoxidase, Western blot of Akt, and gene expression of HMGB1 were measured. The expression of HMGB1 was studied by immunohistochemistry.</p> <p>Results</p> <p>High-tidal-volume ventilation using hyperoxia induced microvascular permeability, Akt activation, HMGB1 mRNA expression, neutrophil infiltration, oxygen radicals, HMGB1 production, and positive staining of Akt in bronchial epithelium. Hyperoxia-induced augmentation of ventilator-induced lung injury was attenuated with Akt deficient mice and pharmacological inhibition of Akt activity by enoxaparin.</p> <p>Conclusion</p> <p>These data suggest that enoxaparin attenuates hyperoxia-augmented high-tidal-volume ventilation-induced neutrophil influx and HMGB1 production through inhibition of the Akt pathway. Understanding the protective mechanism of enoxaparin related with the reduction of HMGB1 may help further knowledge of the effects of mechanical forces in the lung and development of possible therapeutic strategies involved in acute lung injury.</p

Особенности нервно - психического развития детей с билиарной атрезией после трансплантации печени

Background. In young children, the most common liver disease leading to transplantation is biliary atresia. Liver transplantation has fundamentally improved the survival rate of children with biliary atresia. Studies on developmental outcomes in children are mostly limited to small samples; there are no such studies in the Russian Federation.Objective: to determine the cognitive outcomes in children undergoing one-stage or two-stage surgical treatment of biliary atresia.Materials and Methods. 83 children were divided into groups: 36 children underwent transplantation without previous surgical interventions (group 1), 47 children underwent the Kasai palliative portoenterostomy (group 2). Inclusion criteria: 24 months of age or younger at the moment of transplantation, no medical history of neurological pathology. All children were examined before transplantation and at 1, 3, 6 and 12 months after liver transplantation. Psychomotor development was assessed using the Griffiths Psychomotor Development Scale for children under 24 months (translated by E.S. Keshishian), the Griffiths Intellectual Development Scale for children aged 2 to 8 years, and the Modified Checklist for Autism in Toddlers, Revised, for children 16-30 months old.Results. All children had developmental delays at the time of transplantation. Up to 50% of the children had signs of cachexia, with a shoulder circumference of less than 3 percentile. Only two children showed obvious hepatic encephalopathy in the form of depressed consciousness. After liver transplantation, 94% of group 1 children recovered their preoperative psychomotor development levels, and only 68% in group 2 made these gains. At 3 and 6 months after transplantation, about 80% of group 1 children showed normal psychomotor development, whereas in group 2, only 61% did. By 12 months after liver transplantation, the difference between the groups was more evident: 83.3% of group 1 children and only 53.2% of group 2 children were developing according to age. The difference between the groups was statistically significant (p &lt; 0.05).Conclusion. Children who received one-stage treatment of biliary atresia and underwent liver transplantation have better neuropsychological development within a year after surgery than children with two-stage surgical treatment.Актуальность. Билиарная атрезия – наиболее частое показание к трансплантации печени в детском возрасте. Трансплантация печени позволила принципиально повысить выживаемость детей с билиарной атрезией. Исследования исходов развития детей в основном ограничиваются малыми выборками, а в РФ отсутствуют полностью.Цель. Определить когнитивные исходы у детей перенёсших  одноэтапное или двухэтапное хирургическое лечение билиарной атрезии.Материалы и методы. 83 ребёнка были разделены на группы: 36 детям проведена трансплантация без предшествующих хирургических вмешательств (группа 1), 47 детей прошли паллиативный этап портоэнтеростомии по Касаи (группа 2). Критерии включения: возраст на момент трансплантации до 24 мес, отсутствие неврологической патологии в анамнезе.  Все дети осматривались до трансплантации и в период 1,3,6 и 12 мес после трансплантации печени. Оценка психомоторного развития проводилась с использованием Шкалы психомоторного развития по Гриффитс для детей до 24 месяцев (перевод Кешишян Е.С.), Шкалы Интеллектуального Развития по Гриффитс  для детей от 2 до 8 лет, и Модифицированного теста на аутизм, пересмотренного, для детей 16-30 мес. Результаты. Все дети на момент трансплантации имели задержку развития. До 50% детей имели признаки кахексии, окружность плеча была менее 3 перцентиля. Только у двух детей была выявлена явная печёночная энцефалопатия в виде угнетения сознания. После трансплантации печени   94% детей группы 1 восстановили дооперационный уровень психомоторного развития, и только 68% в группе 2 достигли этих успехов. Через 3 и 6 мес после трансплантации около 80 % детей группы 1 демонстрировали нормальное психомоторное развития, тогда как в группе 2 только 61%. К 12 мес после трансплантации печени разница между группами стала более очевидной: 83,3% детей группы 1 и только 53,2 % детей группы 2 развивались по возрасту. Разница между группами была статистически значима (p&lt;0,05).Заключение: Дети  получившие одноэтапное лечение билиарной атрезии, перенёсшие транплантацию печени, имеют лучшие показатели нервно-психического развития в течение года после операции по сравнению с детьми с двухэтапным хирургическом лечением