CLASSIFICATIONS OF INNOVATIONS: APPROACHES AND CONSEQUENCES

Abstract TABAS, J., BERANOVÁ, M., POLÁK, J.: Classifi cation of innovations: approaches and consequences. Acta univ. agric. et silvic. Mendel. Brun., 2011, LIX, No. 2, pp. 399-406 Currently, innovations are perceived as a life blood of businesses. The inevitable fact is that even if the innovations have a potential to transform the companies or all the industries, the innovations are high risky. Even though, the second fact is that in order to companies' development and their survival on the markets, the innovations have become the necessity. In the theory, it is rather diffi cult to fi nd a comprehensive defi nition of innovation, and to settle down a general defi nition of innovation becomes more and more diffi cult with the growing number of domains where the innovations, or possible innovations start to appear in a form of added value to something that already exist. Defi nition of innovation has come through a long process of development; from early defi nition of Schumpeter who has connected innovation especially with changes in products or production processes, to recent defi nitions based on the added value for a society. One of possible approaches to defi ne the content of innovation is to base the defi nition on classifi cation of innovation. In the article, the authors provide the analysis of existing classifi cations of innovations in order to fi nd, respectively in order to defi ne the general content of innovation that would confi rm (or reject) their defi nition of innovation derived in the frame of their previous work where they state that innovation is a change that leads to gaining profi t for an individual, for business entity, or for society, while the profi t is not only the accounting one, but it is the economic profi t. The article is based especially on the secondary research while the authors employ the method of analysis with the aim to confront various classifi cation-based defi nitions of innovation. Then the methods used are especially comparison, analysis and synthesis. added value, classifi cation of innovations, competitive advantage, defi nition of innovation, innovatio

Circulation first – the time has come to question the sequencing of care in the ABCs of trauma; an American Association for the Surgery of Trauma multicenter trial

Background The traditional sequence of trauma care: Airway, Breathing, Circulation (ABC) has been practiced for many years. It became the standard of care despite the lack of scientific evidence. We hypothesized that patients in hypovolemic shock would have comparable outcomes with initiation of bleeding treatment (transfusion) prior to intubation (CAB), compared to those patients treated with the traditional ABC sequence. Methods This study was sponsored by the American Association for the Surgery of Trauma multicenter trials committee. We performed a retrospective analysis of all patients that presented to trauma centers with presumptive hypovolemic shock indicated by pre-hospital or emergency department hypotension and need for intubation from January 1, 2014 to July 1, 2016. Data collected included demographics, timing of intubation, vital signs before and after intubation, timing of the blood transfusion initiation related to intubation, and outcomes. Results From 440 patients that met inclusion criteria, 245 (55.7%) received intravenous blood product resuscitation first (CAB), and 195 (44.3%) were intubated before any resuscitation was started (ABC). There was no difference in ISS, mechanism, or comorbidities. Those intubated prior to receiving transfusion had a lower GCS than those with transfusion initiation prior to intubation (ABC: 4, CAB:9, p = 0.005). Although mortality was high in both groups, there was no statistically significant difference (CAB 47% and ABC 50%). In multivariate analysis, initial SBP and initial GCS were the only independent predictors of death. Conclusion The current study highlights that many trauma centers are already initiating circulation first prior to intubation when treating hypovolemic shock (CAB), even in patients with a low GCS. This practice was not associated with an increased mortality. Further prospective investigation is warranted. Trial registration IRB approval number: HM20006627. Retrospective trial not registered

IRE1β Inhibits Chylomicron Production by Selectively Degrading MTP mRNA

SummaryMicrosomal triglyceride transfer protein (MTP) is needed to assemble chylomicrons in the endoplasmic reticulum (ER) of enterocytes. We explored the role of an ER stress protein, inositol-requiring enzyme 1β (IRE1β), in regulating this process. High-cholesterol and high-fat diets decreased intestinal IRE1β mRNA in wild-type mice. Ire1b−/− mice fed high-cholesterol and high-fat diets developed more pronounced hyperlipidemia because these mice secreted more chylomicrons and expressed more intestinal MTP, though not hepatic MTP, than wild-type mice did. Chylomicron secretion and MTP expression also were increased in primary enterocytes isolated from cholesterol-fed Ire1b−/− mice. There was no correlation between ER stress and MTP expression. Instead, cell culture studies revealed that IRE1β, but not its ubiquitous homolog IRE1α, decreased MTP mRNA through increased posttranscriptional degradation. Conversely, knockdown of IRE1β enhanced MTP expression. These studies show that IRE1β plays a role in regulating MTP and in chylomicron production

Modeling and MEG evidence of early consonance processing in auditory cortex

Pitch is a fundamental attribute of auditory perception. The interaction of concurrentpitches gives rise to a sensation that can be characterized by its degree of consonance ordissonance. In this work, we propose that human auditory cortex (AC) processes pitchand consonance through a common neural network mechanism operating at earlycortical levels. First, we developed a new model of neural ensembles incorporatingrealistic neuronal and synaptic parameters to assess pitch processing mechanisms atearly stages of AC. Next, we designed a magnetoencephalography (MEG) experiment tomeasure the neuromagnetic activity evoked by dyads with varying degrees ofconsonance or dissonance. MEG results show that dissonant dyads evoke a pitch onsetFebruary 15, 20191/44 response (POR) with a latency up to 36 ms longer than consonant dyads. Additionally,we used the model to predict the processing time of concurrent pitches; here, consonantpitch combinations were decoded faster than dissonant combinations, in line with theexperimental observations. Specifically, we found a striking match between thepredicted and the observed latency of the POR as elicited by the dyads. These novelresults suggest that consonance processing starts early in human auditory cortex andmay share the network mechanisms that are responsible for (single) pitch processing

Forkhead Transcription Factors (FoxOs) Promote Apoptosis of Insulin-Resistant Macrophages During Cholesterol-Induced Endoplasmic Reticulum Stress

OBJECTIVE—Endoplasmic reticulum stress increases macrophage apoptosis, contributing to the complications of atherosclerosis. Insulin-resistant macrophages are more susceptible to endoplasmic reticulum stress–associated apoptosis probably contributing to macrophage death and necrotic core formation in atherosclerotic plaques in type 2 diabetes. However, the molecular mechanisms of increased apoptosis in insulin-resistant macrophages remain unclear

Can we identify non-stationary dynamics of trial-to-trial variability?"

Identifying sources of the apparent variability in non-stationary scenarios is a fundamental problem in many biological data analysis settings. For instance, neurophysiological responses to the same task often vary from each repetition of the same experiment (trial) to the next. The origin and functional role of this observed variability is one of the fundamental questions in neuroscience. The nature of such trial-to-trial dynamics however remains largely elusive to current data analysis approaches. A range of strategies have been proposed in modalities such as electro-encephalography but gaining a fundamental insight into latent sources of trial-to-trial variability in neural recordings is still a major challenge. In this paper, we present a proof-of-concept study to the analysis of trial-to-trial variability dynamics founded on non-autonomous dynamical systems. At this initial stage, we evaluate the capacity of a simple statistic based on the behaviour of trajectories in classification settings, the trajectory coherence, in order to identify trial-to-trial dynamics. First, we derive the conditions leading to observable changes in datasets generated by a compact dynamical system (the Duffing equation). This canonical system plays the role of a ubiquitous model of non-stationary supervised classification problems. Second, we estimate the coherence of class-trajectories in empirically reconstructed space of system states. We show how this analysis can discern variations attributable to non-autonomous deterministic processes from stochastic fluctuations. The analyses are benchmarked using simulated and two different real datasets which have been shown to exhibit attractor dynamics. As an illustrative example, we focused on the analysis of the rat's frontal cortex ensemble dynamics during a decision-making task. Results suggest that, in line with recent hypotheses, rather than internal noise, it is the deterministic trend which most likely underlies the observed trial-to-trial variability. Thus, the empirical tool developed within this study potentially allows us to infer the source of variability in in-vivo neural recordings

An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques

Chronic unresolved inflammation plays a causal role in the development of advanced atherosclerosis, but the mechanisms that prevent resolution in atherosclerosis remain unclear. Here, we use targeted mass spectrometry to identify specialized pro-resolving lipid mediators (SPM) in histologically-defined stable and vulnerable regions of human carotid atherosclerotic plaques. The levels of SPMs, particularly resolvin D1 (RvD1), and the ratio of SPMs to pro-inflammatory leukotriene B4 (LTB₄), are significantly decreased in the vulnerable regions. SPMs are also decreased in advanced plaques of fat-fed Ldlr⁻/⁻ mice. Administration of RvD1 to these mice during plaque progression restores the RvD1:LTB₄ ratio to that of less advanced lesions and promotes plaque stability, including decreased lesional oxidative stress and necrosis, improved lesional efferocytosis, and thicker fibrous caps. These findings provide molecular support for the concept that defective inflammation resolution contributes to the formation of clinically dangerous plaques and offer a mechanistic rationale for SPM therapy to promote plaque stability

Діагностика цитолітичного синдрому у хворих на туберкульоз легень

Introduction. The liver is one of the most important organs of the human body, performing a number of important functions. Among the common liver diseases, infiltrative pathologies we distinguished: fatty degeneration, lymphomas, amyloidosis, sarcoidosis and tuberculosis. Characterizing liver disease, the manifestations of disorders are divided into syndromes that help to diagnose a particular disease of the liver and determine its causes. In particular – the cytolytic syndrome (CS).The aim of the study – to examine the CS markers in the case of liver dysfunction in patients with newly diagnosed lung tuberculosis prior to treatment and after two months of therapy with first-line anti-tuberculosis drugs.Methods of the research. Two groups of people were examined: the 1st control group of practically healthy donors – 34 people; and the 2nd – patients with newly diagnosed pulmonary tuberculosis prior to treatment and after two months of therapy with first-line anti-tuberculosis drugs (31 people). All patients underwent standard biochemical blood tests, ultrasound of the liver in dynamics. The spectrum of biochemical blood test parameters included determination of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and γ-glutamyltranspeptidase (GGTP).Results and Discussion. The obtained data testifying to occurrence of CS in newly diagnosed tuberculosis patients before the start of treatment are confirmed by the tendency to increase the levels of AST and GGTP. Especially such changes are observed after intensive therapy with antituberculous drugs. There are likely changes in such markers as ALT, LDH and GGTP.Conclusions. It is established that tuberculous intoxication can affect the functional state of the liver. After prolonged treatment of patients with pulmonary tuberculosis, an increase in the indices of such markers of cytolysis as ALT, LDH and GGTP is observed. Disturbance of liver function during therapy may be due to the hepatotoxic effect of anti-tuberculosis drugs, which necessitates the appointment for patients hepatoprotectors.Вступление. Печень является одним из важнейших органов тела человека и выполняет ряд важнейших функций. Среди распространенных заболеваний печени выделяют инфильтративные патологии: жировую дистрофию, лимфомы, амилоидоз, саркоидоз и туберкулез. Характеризуя болезни печени, проявления расстройств принято разделять на синдромы, которые помогают диагностировать то или иное заболевание этого органа и определить его причины. В частности, выделяют цитолитический синдром (ЦС).Цель исследования – изучить маркеры ЦС при нарушении функции печени у больных с впервые диагностированным туберкулезом легких до лечения и через два месяца терапии противотуберкулезными препаратами первого ряда.Методы исследования. Было обследовано две группы лиц: 1-я (контрольная) – практически здоровые доноры (34 человека); 2-я – больные с впервые диагностированным туберкулезом легких до лечения и через два месяца терапии противотуберкулезными препаратами первого ряда (31 человек). Всем пациентам проводили стандартные биохимические исследования крови, УЗИ печени в динамике. Спектр показателей биохимического исследования крови включал определение аланинаминотрансферазы (АлАТ), аспартатаминотрансферазы (АсАТ), лактатдегидрогеназы (ЛДГ) и γ-глутамилтранспептидазы (ГГТП).Результаты и обсуждение. Полученные данные, свидетельствующие о возникновении ЦС у больных с впервые диагностированным туберкулезом до начала лечения, подтверждаются тенденцией к увеличению уровней АсАТ и ГГТП. Особенно такие изменения наблюдали после интенсивной терапии противотуберкулезными препаратами. Отмечали вероятные изменения таких маркеров, как АлАТ, ЛДГ и ГГТП.Выводы. Установлено, что туберкулезная интоксикация может влиять на функциональное состояние печени. После длительного лечения больных туберкулезом легких отмечают увеличение показателей таких маркеров цитолиза, как АлАТ, ЛДГ и ГГТП. Нарушения функции печени во время терапии могут быть вызваны гепатотоксическим действием противотуберкулезных препаратов, что обусловливает необходимость назначения больным гепатопротекторов.Вступ. Печінка є одним із найважливіших органів тіла людини і виконує низку надзвичайно важливих функцій. Серед поширених захворювань печінки виділяють інфільтративні патології: жирову дистрофію, лімфоми, амілоїдоз, саркоїдоз і туберкульоз. Характеризуючи хвороби печінки, прояви розладів прийнято розділяти на синдроми, які допомагають діагностувати те чи інше захворювання цього органа та визначити його причини. Зокрема, виділяють цитолітичний синдром (ЦС).Мета дослідження – вивчити маркери ЦС при порушенні функції печінки у хворих на вперше діагностований туберкульоз легень до лікування і через два місяці терапії протитуберкульозними препаратами першого ряду.Методи дослідження. Було обстежено дві групи осіб: 1-ша контрольна – практично здорові донори – (34 особи); 2-га – хворі на вперше діагностований туберкульоз легень до лікування і через два місяці терапії протитуберкульозними препаратами першого ряду (31 особа). Усім пацієнтам проводили стандартні біохімічні дослідження крові, УЗД печінки в динаміці. Спектр показників біохімічного дослідження крові включав визначення аланінамінотрансферази (АлАТ), аспартатамінотрансферази (АсАТ), лактатдегідрогенази (ЛДГ) та γ-глутамілтранспептидази (ГГТП).Результати й обговорення. Отримані дані, які свідчили про виникнення ЦС у хворих на вперше діагностований туберкульоз до початку лікування, підтверджувалися тенденцією до збільшення рівнів АсАТ і ГГТП. Особливо такі зміни спостерігали після інтенсивної терапії протитуберкульозними препаратами. Відмічали вірогідні зміни таких маркерів, як АлАТ, ЛДГ і ГГТП.Висновки. Встановлено, що туберкульозна інтоксикація може впливати на функціональний стан печінки. Після тривалого лікування хворих на туберкульоз легень відмічають збільшення показників таких маркерів цитолізу, як АлАТ, ЛДГ і ГГТП. Порушення функції печінки під час терапії можуть бути спричинені гепатотоксичною дією протитуберкульозних препаратів, що зумовлює необхідність призначення хворим гепатопротекторів.