ІННОВАЦІЙНІ НАПРЯМИ МОДЕЛЮВАННЯ ОСОБИ НЕВІДОМОГО ЗЛОЧИНЦЯ В ДІЯЛЬНОСТІ ОРГАНІВ КРИМІНАЛЬНОЇ ЮСТИЦІЇ

The innovative directions of modeling personality of an unknown criminal are considered. An attempt was made to clarify the essence of such innovative directions, used in the activities of criminal justice authorities. The theoretical foundations of the use of innovative approaches in the modeling of the person of an unknown criminal in the activities of the criminal justice authorities are determined.Розглянуто інноваційні напрями моделювання особи невідомого злочинця. Здійснено спробу з’ясувати сутність таких інноваційних напрямів, що використовуються в діяльності органів кримінальної юстиції. Визначено теоретичні засади використання інноваційних підходів під час моделювання особи невідомого злочинця в діяльності органів кримінальної юстиції

ІМПЛЕМЕНТАЦІЯ СИМУЛЯЦІЙНОГО ТРЕНІНГУ НАДАННЯ НЕВІДКЛАДНОЇ ДОПОМОГИ ДЛЯ СТУДЕНТІВ 6 КУРСУ ПРИ ВИВЧЕННІ ДИСЦИПЛІНИ “ВНУТРІШНЯ МЕДИЦИНА” (ОГЛЯД ЛІТЕРАТУРИ ТА ВЛАСНИЙ ДОСВІД)

The aim of the work – to analyze, generalize existing points of view in the education system, which affect the issue of necessity, effectiveness and features of the simulation programs use for medical students. The main body. An overview of modern literature on the implementation of simulation methods in medical education. Simulation training is one of the effective ways to learn how to manage errors. Simulation training allows to learn how to work in accordance with modern algorithms for diagnosis and emergency care, to develop team interaction and coordination, to increase the level of implementation of complex medical manipulations and to evaluate the effectiveness of their own actions. In particular, at the Internal Medicine Department No. 3 of Dnipropetrovsk Medical Academy a method of simulation training is developed  involving university staff as “standardized patients” for modeling clinical situations of differentiation and assistance in various urgent states. Conclusions. In our view, this implementation of the simulation training is a valuable tool for improving the professional skills of medical students. Elements of this technique are applicable at different stages of educational activity: not only in the development of skills in emergency care, but also during the final certification of the 6th year students.Мета роботи – аналіз, узагальнення існуючих точок зору в системі освіти, які торкаються питання про необхідність, ефективність та особливості використання симуляційних програм навчання студентів-медиків. Основна частина. Проведено огляд сучасної літератури по впровадженню симуляційних методів навчання в медичній освіті. Симуляційне навчання є одним з ефективних способів навчитися керувати помилками. Симуляційне навчання дозволяє навчатися працювати відповідно до сучасних алгоритмів діагностики та надання невідкладної допомоги, виробити командну взаємодію та координацію, підвищити рівень виконання складних медичних маніпуляцій та оцінити ефективність власних дій. Зокрема, в ДЗ “ДМА МОЗ України” на кафедрі внутрішньої медицини 3 розроблена методика імітаційного навчання із залученням співробітників ВНЗ в якості стандартизованих пацієнтів для моделювання клінічних ситуацій диференціації та надання допомоги при різних невідкладних станах. Висновки. На наш погляд, дана імплементація симуляційного тренінгу є цінним інструментом вдосконалення професійних навичок студентів медичних вузів. Елементи даної методики застосовні на різних етапах освітньої діяльності: не тільки при відпрацюванні навичок невідкладної допомоги, а також при проведенні підсумкової атестації студентів 6 курсу

ОСОБЛИВОСТІ ГАЗОРОЗРЯДНОГО СВІТІННЯ ПАЛЬЦІВ РУК ЛЮДИНИ ПРИ РІЗНИХ ТИПАХ ЕНЕРГЕТИЧНОЇ АКТИВНОСТІ

There were 52 healthy people. Of them, 28 were in junior courses and 24 were in senior courses. According to the results of psychological tests there were identified three types of thinking: visual-figurative and verbal-logical, intuitive. Kirlian photographs of the surveyed individuals fingers in the experimental device «REC 1» were done. The method of acquiring, processing, and subsequent analysis included analog-to-digital conversion Kirlian images to highlight areas of illumination of the individual fingers, binarization of images with the threshold brightness, calculation of the area of corona glow. The obtained results complemented results of psychological tests, revealed mixed types of thinking, their expression, the dependence of the period of study at the university. To identify the emotional characteristics of the students associated with the constitutional type of the individual, selectively kronograf research on Polarod color photographic film with computer processing of scanned images carried out. Check radiation around the fingers of people surveyed in the color film, determination of the ratios of colors in the image, their energy allowed to determine the type of emotional activation of student body's potential abilities that affects motivation and optimize learning at the university.Обследовано 52 практически здоровых студента. Из них 28 человек обучались на младших курсах и 24 — студенты старших курсов. По результатам психологических тестов определяли три типа мышления: наглядно-образное, словесно-логическое, интуитивное. Проводили кирлиан-фотографирование пальцев рук обследуемых на экспериментальном приборе «РЕК 1». Методы регистрации, обработки и последующего анализа включали аналого-цифровое преобразование кирлиановских изображений с целью выделения областей свечения отдельных пальцев, бинаризацию изображений за порогом яркости свечения, вычисление площади короны свечения. Полученные результаты дополнили результаты психологических тестов, выявили смешанные типы мышления, их выраженность, зависимость от срока обучения в университете. Для выявления психоэмоциональных особенностей студентов, связанных с конституционным типом личности, проводили выборочно кирлианографическое исследование на цветной фотопленке «Поляроид» с компьютерной обработкой отсканированных изображений. Регистрация на цветной фотопленке излучения вокруг пальцев рук обследованных, определение соотношений цветов изображения, их энергетики позволило определить тип психоэмоциональной активации организма и собственные потенциальные способности студента, что влияет на мотивацию и оптимизацию обучения в университете.Обстежено 52 практично здорових студенти. З них 28 осіб були молодших курсів навчання та 24 — студенти старших курсів. За результатами психологічних тестів визначали три типи мислення: наочно-образне, словесно-логічне, інтуїтивне. Проводили кірліан-фотографування пальців рук обстежуваних осіб на експериментальному приладі «РЕК 1». Методи реєстрації, обробки та подальшого аналізу включали аналого-цифрове перетворення кірліанівських зображень з метою виділення областей світіння окремих пальців, бінаризацію зображень за порогом яскравості світіння, обчислення площі корони світіння. Отримані результати доповнили результати психологічних тестів, виявили змішані типи мислення, їх виразність, залежність від терміну навчання в університеті. Для виявлення психоемоційних особливостей студентів, пов'язаних із конституційним типом особистості, проводили вибірково кірліанографічне дослідження на кольоровій фотоплівці «Поляроїд» із комп'ютерним обробленням відсканованих зображень. Реєстрація на кольоровій фотоплівці випромінювання навколо пальців рук обстежених осіб, визначення співвідношень кольорів зображення, їх енергетики дозволили визначити тип психоемоційної активації організму та потенційні власні здібності студента, що вливають на мотивацію й оптимізацію навчання в університеті

Mitogen- and Stress-Activated Protein Kinase 1 Regulates Status Epilepticus-Evoked Cell Death in the Hippocampus

Mitogen-activated protein kinase (MAPK) signaling has been implicated in a wide range of neuronal processes, including development, plasticity, and viability. One of the principal downstream targets of both the extracellular signal-regulated kinase/MAPK pathway and the p38 MAPK pathway is M itogen- and S tress-activated protein K inase 1 (MSK1). Here, we sought to understand the role that MSK1 plays in neuroprotection against excitotoxic stimulation in the hippocampus. To this end, we utilized immunohistochemical labeling, a MSK1 null mouse line, cell viability assays, and array-based profiling approaches. Initially, we show that MSK1 is broadly expressed within the major neuronal cell layers of the hippocampus and that status epilepticus drives acute induction of MSK1 activation. In response to the status epilepticus paradigm, MSK1 KO mice exhibited a striking increase in vulnerability to pilocarpine-evoked cell death within the CA1 and CA3 cell layers. Further, cultured MSK1 null neurons exhibited a heighted level of N-methyl-D-aspartate-evoked excitotoxicity relative to wild-type neurons, as assessed using the lactate dehydrogenase assay. Given these findings, we examined the hippocampal transcriptional profile of MSK1 null mice. Affymetrix array profiling revealed that MSK1 deletion led to the significant (>1.25-fold) downregulation of 130 genes and an upregulation of 145 genes. Notably, functional analysis indicated that a subset of these genes contribute to neuroprotective signaling networks. Together, these data provide important new insights into the mechanism by which the MAPK/MSK1 signaling cassette confers neuroprotection against excitotoxic insults. Approaches designed to upregulate or mimic the functional effects of MSK1 may prove beneficial against an array of degenerative processes resulting from excitotoxic insults

Role of Palladin Phosphorylation by Extracellular Signal-Regulated Kinase in Cell Migration

Phosphorylation of actin-binding proteins plays a pivotal role in the remodeling of the actin cytoskeleton to regulate cell migration. Palladin is an actin-binding protein that is phosphorylated by growth factor stimulation; however, the identity of the involved protein kinases remains elusive. In this study, we report that palladin is a novel substrate of extracellular signal-regulated kinase (ERK). Suppression of ERK activation by a chemical inhibitor reduced palladin phosphorylation, and expression of active MEK alone was sufficient for phosphorylation. In addition, an in vitro kinase assay demonstrated direct palladin phosphorylation by ERK. We found that Ser77 and Ser197 are essential residues for phosphorylation. Although the phosphorylation of these residues was not required for actin cytoskeletal organization, we found that expression of non-phosphorylated palladin enhanced cell migration. Finally, we show that phosphorylation inhibits the palladin association with Abl tyrosine kinase. Taken together, our results indicate that palladin phosphorylation by ERK has an anti-migratory function, possibly by modulating interactions with molecules that regulate cell migration

The cytokine tumor necrosis factor-like weak inducer of apoptosis and its receptor fibroblast growth factor-inducible 14 have a neuroprotective effect in the central nervous system

<p>Abstract</p> <p>Background</p> <p>Cerebral cortical neurons have a high vulnerability to the harmful effects of hypoxia. However, the brain has the ability to detect and accommodate to hypoxic conditions. This phenomenon, known as preconditioning, is a natural adaptive process highly preserved among species whereby exposure to sub-lethal hypoxia promotes the acquisition of tolerance to a subsequent lethal hypoxic injury. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are found in neurons and their expression is induced by exposure to sub-lethal hypoxia. Accordingly, in this work we tested the hypothesis that the interaction between TWEAK and Fn14 induces tolerance to lethal hypoxic and ischemic conditions.</p> <p>Methods</p> <p>Here we used <it>in vitro </it>and <it>in vivo </it>models of hypoxic and ischemic preconditioning, an animal model of transient middle cerebral artery occlusion and mice and neurons genetically deficient in TWEAK, Fn14, or tumor necrosis factor alpha (TNF-α) to investigate whether treatment with recombinant TWEAK or an increase in the expression of endogenous TWEAK renders neurons tolerant to lethal hypoxia. We used enzyme-linked immunosorbent assay to study the effect of TWEAK on the expression of neuronal TNF-α, Western blot analysis to investigate whether the effect of TWEAK was mediated by activation of mitogen-activated protein kinases and immunohistochemical techniques and quantitative real-time polymerase chain reaction analysis to study the effect of TWEAK on apoptotic cell death.</p> <p>Results</p> <p>We found that either treatment with recombinant TWEAK or an increase in the expression of TWEAK and Fn14 induce hypoxic and ischemic tolerance <it>in vivo </it>and <it>in vitro</it>. This protective effect is mediated by neuronal TNF-α and activation of the extracellular signal-regulated kinases 1 and 2 pathway via phosphorylation and inactivation of the B-cell lymphoma 2-associated death promoter protein.</p> <p>Conclusions</p> <p>Our work indicate that the interaction between TWEAK and Fn14 triggers the activation of a cell signaling pathway that results in the induction of tolerance to lethal hypoxia and ischemia. These data indicate that TWEAK may be a potential therapeutic strategy to protect the brain from the devastating effects of an ischemic injury.</p

Distinct Expression/Function of Potassium and Chloride Channels Contributes to the Diverse Volume Regulation in Cortical Astrocytes of GFAP/EGFP Mice

Recently, we have identified two astrocytic subpopulations in the cortex of GFAP-EGFP mice, in which the astrocytes are visualized by the enhanced green–fluorescent protein (EGFP) under the control of the human glial fibrillary acidic protein (GFAP) promotor. These astrocytic subpopulations, termed high response- (HR-) and low response- (LR-) astrocytes, differed in the extent of their swelling during oxygen-glucose deprivation (OGD). In the present study we focused on identifying the ion channels or transporters that might underlie the different capabilities of these two astrocytic subpopulations to regulate their volume during OGD. Using three-dimensional confocal morphometry, which enables quantification of the total astrocytic volume, the effects of selected inhibitors of K+ and Cl− channels/transporters or glutamate transporters on astrocyte volume changes were determined during 20 minute-OGD in situ. The inhibition of volume regulated anion channels (VRACs) and two-pore domain potassium channels (K2P) highlighted their distinct contributions to volume regulation in HR-/LR-astrocytes. While the inhibition of VRACs or K2P channels revealed their contribution to the swelling of HR-astrocytes, in LR-astrocytes they were both involved in anion/K+ effluxes. Additionally, the inhibition of Na+-K+-Cl− co-transporters in HR-astrocytes led to a reduction of cell swelling, but it had no effect on LR-astrocyte volume. Moreover, employing real-time single-cell quantitative polymerase chain reaction (PCR), we characterized the expression profiles of EGFP-positive astrocytes with a focus on those ion channels and transporters participating in astrocyte swelling and volume regulation. The PCR data revealed the existence of two astrocytic subpopulations markedly differing in their gene expression levels for inwardly rectifying K+ channels (Kir4.1), K2P channels (TREK-1 and TWIK-1) and Cl− channels (ClC2). Thus, we propose that the diverse volume changes displayed by cortical astrocytes during OGD mainly result from their distinct expression patterns of ClC2 and K2P channels

Regulation of cellular proliferation, differentiation and cell death by activated Raf

The protein kinases Raf-1, A-Raf and B-Raf connect receptor stimulation with intracellular signaling pathways and function as a central intermediate in many signaling pathways. Gain-of-function experiments shed light on the pleiotropic biological activities of these enzymes. Expression experiments involving constitutively active Raf revealed the essential functions of Raf in controlling proliferation, differentiation and cell death in a cell-type specific manner

Nucleologenesis in the Caenorhabditis elegans Embryo

In the Caenorhabditis elegans nematode, the oocyte nucleolus disappears prior to fertilization. We have now investigated the re-formation of the nucleolus in the early embryo of this model organism by immunostaining for fibrillarin and DAO-5, a putative NOLC1/Nopp140 homolog involved in ribosome assembly. We find that labeled nucleoli first appear in somatic cells at around the 8-cell stage, at a time when transcription of the embryonic genome begins. Quantitative analysis of radial positioning showed the nucleolus to be localized at the nuclear periphery in a majority of early embryonic nuclei. At the ultrastructural level, the embryonic nucleolus appears to be composed of a relatively homogenous core surrounded by a crescent-shaped granular structure. Prior to embryonic genome activation, fibrillarin and DAO-5 staining is seen in numerous small nucleoplasmic foci. This staining pattern persists in the germline up to the ∼100-cell stage, until the P4 germ cell divides to give rise to the Z2/Z3 primordial germ cells and embryonic transcription is activated in this lineage. In the ncl-1 mutant, which is characterized by increased transcription of rDNA, DAO-5-labeled nucleoli are already present at the 2-cell stage. Our results suggest a link between the activation of transcription and the initial formation of nucleoli in the C. elegans embryo

MPP+-induced cytotoxicity in neuroblastoma cells: Antagonism and reversal by guanosine

Guanosine exerts neuroprotective effects in the central nervous system. Apoptosis, a morphological form of programmed cell death, is implicated in the pathophysiology of Parkinson’s disease (PD). MPP+, a dopaminergic neurotoxin, produces in vivo and in vitro cellular changes characteristic of PD, such as cytotoxicity, resulting in apoptosis. Undifferentiated human SH-SY5Y neuroblastoma cells had been used as an in vitro model of Parkinson’s disease. We investigated if extracellular guanosine affected MPP+-induced cytotoxicity and examined the molecular mechanisms mediating its effects. Exposure of neuroblastoma cells to MPP+ (10 μM–5 mM for 24–72 h) induced DNA fragmentation in a time-dependent manner (p < 0.05). Administration of guanosine (100 μM) before, concomitantly with or, importantly, after the addition of MPP+ abolished MPP+-induced DNA fragmentation. Addition of MPP+ (500 μM) to cells increased caspase-3 activity over 72 h (p < 0.05), and this was abolished by pre- or co-treatment with guanosine. Exposure of cells to pertussis toxin prior to MPP+ eliminated the anti-apoptotic effect of guanosine, indicating that this effect is dependent on a Gi protein-coupled receptor, most likely the putative guanosine receptor. The protection by guanosine was also abolished by the selective inhibitor of the enzyme PI-3-K/Akt/PKB (LY294002), confirming that this pathway plays a decisive role in this effect of guanosine. Neither MPP+ nor guanosine had any significant effect on α-synuclein expression. Thus, guanosine antagonizes and reverses MPP+-induced cytotoxicity of neuroblastoma cells via activation of the cell survival pathway, PI-3-K/Akt/PKB. Our results suggest that guanosine may be an effective pharmacological intervention in PD