МОДЕЛЮВАННЯ ПРОЦЕСУ БЕЗОПЛАТНОГО ЗАБЕЗПЕЧЕННЯ ІНСУЛІНОМ ПАЦІЄНТІВ ІЗ ДІАГНОЗОМ ЦУКРОВИЙ ДІАБЕТ ІЗ ВИКОРИСТАННЯМ МЕТОДОЛОГІЇ STRUCTURE ANALYSIS AND DESIGN TECHNIQUE

The goal of the current project is the model creation for providing free prescript of insulin distribution with smart-car d usage based on the Cabinet of Ministers of Ukraine Resolution from 17.08.1998 № 1303. The work includes model creation with a help of system analysis tools (Structure Analysis and D esign Technique, SADT) by IDEF0-notation and CA BPwin 4.0 software usage.Описана модель обеспечения льготного (бесплатного) отпуска инсулина по рецептам врачей с использованием смарт-карт. Работа включает в себя построение модели средствами системного анализа (Structure Analysis and Design Technique, SADT) с использованием нотации IDEF0 и ПО CA BPwin 4.0.Описана модель забезпечення пільгового (безоплатного) відпуску інсуліну за рецептами лікарів із використанням смарт-карток. Робота включає в себе побудову моделі засобами системного аналізу (Structure Analysis and Design Technique, SADT) із використанням нотації IDEF0 та ПЗ CA BPwin 4.0

Telemedicine as a priority instrument of informational-methodical basis for medical hospitals work

Проведено аналіз понять «телемедицина», а також «телемедичні технології», які сьогодні застосовуються. Автори наводять власні результати участі в телемедичних мостах і проведенні телемедичного консультування. Обговорюються варіанти різних конфігурацій телемедичного обладнання, яке можна використовувати в лікувально-профілактичних закладах України.The analysis of contemporary notions on “telemedicine” and “telemedical technologies” was made. The author delivered his own results of participation in telemedical bridgies and telemedical consultations. Different versions of telemedical devices configurations, which might be explored in Ukrainian hospitals have been also considered

Sleep-wake sensitive mechanisms of adenosine release in the basal forebrain of rodents : an in vitro study

Adenosine acting in the basal forebrain is a key mediator of sleep homeostasis. Extracellular adenosine concentrations increase during wakefulness, especially during prolonged wakefulness and lead to increased sleep pressure and subsequent rebound sleep. The release of endogenous adenosine during the sleep-wake cycle has mainly been studied in vivo with microdialysis techniques. The biochemical changes that accompany sleep-wake status may be preserved in vitro. We have therefore used adenosine-sensitive biosensors in slices of the basal forebrain (BFB) to study both depolarization-evoked adenosine release and the steady state adenosine tone in rats, mice and hamsters. Adenosine release was evoked by high K+, AMPA, NMDA and mGlu receptor agonists, but not by other transmitters associated with wakefulness such as orexin, histamine or neurotensin. Evoked and basal adenosine release in the BFB in vitro exhibited three key features: the magnitude of each varied systematically with the diurnal time at which the animal was sacrificed; sleep deprivation prior to sacrifice greatly increased both evoked adenosine release and the basal tone; and the enhancement of evoked adenosine release and basal tone resulting from sleep deprivation was reversed by the inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. These data indicate that characteristics of adenosine release recorded in the BFB in vitro reflect those that have been linked in vivo to the homeostatic control of sleep. Our results provide methodologically independent support for a key role for induction of iNOS as a trigger for enhanced adenosine release following sleep deprivation and suggest that this induction may constitute a biochemical memory of this state

ИНФЕКЦИИ, ВЫЗВАННЫЕ ACINETOBACTER BAUMANNII, У ОНКОЛОГИЧЕСКИХ БОЛЬНЫХ

The purpose of the study was to evaluate the frequency of isolation of multi-resistant Acinetobacter baumannii in cancer patients and identify the mechanisms of resistance to carbapenems.Material and Methods. We analyzed 942 strains of A. baumannii isolated from clinical samples of cancer patients in the period 2014–16. The level of resistance to ampicillin-sulbactam, piperacillin-tazobactam, ceftazidime, cefepime, imipenem, meropenem, ciprofloxacin, amikacin, and to other antibiotics was determined. Carbapenem-resistant (Car-R) strains were examined for the presence of carbapenemases.Results. Between 2014 and 2016, the number of strains resistant to: ampicillin-sulbactam was 95.5–74.6 % (p≤0.0001), piperacillin – tazobactam 64.3–98.1 % (p<0.01), ceftazidime – 66.1–44.3 % (p≤0.0001), cefepime – 94.7–98.3 % (p≤0.01), ciprofloxacin – 95.8–91.8 % (p<0.05), amikacin – 77.7–91.0 % (p≤0.0001). An increase in the number of Car-R strains from 77.2 % in 2014 to 84.1 % in 2015 (p<0.05) and up to 90.0 % in 2016 (p<0.05) was observed. The resistance to imipenem was 100 %. The analysis of 6 strains in relation to acquired carbapenemases revealed the production of serine carbapenemases of the OXA-23 group in 100 % of cases.Conclusion. A. baumannii remains to be highly resistant to almost all classes of antibiotics, and the resistance to carbapenems is caused by the production of carbapenemases OXA-23.Цель исследования – оценить частоту выделения мультирезистентных Acinetobacter baumannii у онкологических больных и выявить механизмы резистентности к карбапенемам.Материал и методы. Проанализировано 942 штамма A. baumannii, выделенных из патологических материалов от онкологических больных в 2014–16 гг. Определен уровень резистентности к ампициллину-сульбактаму, пиперациллину-тазобактаму, цефтазидиму, цефепиму, имипенему, меропенему, ципрофлоксацину, амикацину и другим антибиотикам в динамике. Резистентные к карбапенемам (Car-R) штаммы исследовали на наличие карбапенемаз.Результаты. Число штаммов, резистентных к ампициллину-сульбактаму, в период с 2014 по 2016 г. составило 95,5–74,6 % (p≤0,0001), пиперациллину/тазобактаму – 64,3–98,1 % (p<0,01), цефтазидиму – 66,1–44,3 % (p≤0,0001), цефепиму – 94,7–98,3 % (p≤0,01), ципрофлоксацину – 95,8–91,8 % (p<0,05), амикацину – 77,7–91,0 % (p≤0,0001). В то же время наблюдалось увеличение числа Car-R (меронем-резистентных) штаммов с 77,2 % в 2014 г. до 84,1 % в 2015 г. (p<0,05) и до 90,0 % в 2016 г. (p<0,05). К имипенему резистентность составляла 100 %. Анализ 6 штаммов в отношении приобретенных карбапенемаз выявил продукцию сериновых карбапенемаз группы OXA-23 в 100 % случаев.Заключение. A. baumannii сохраняет высокую устойчивость к практически всем классам антибиотиков, причем устойчивость к карбапенемам обусловлена продукцией карбапенемаз OXA-23 и достоверно увеличилась в динамике с 2014 по 2016 г

cGMP-Dependent Protein Kinase Type I Is Implicated in the Regulation of the Timing and Quality of Sleep and Wakefulness

Many effects of nitric oxide (NO) are mediated by the activation of guanylyl cyclases and subsequent production of the second messenger cyclic guanosine-3′,5′-monophosphate (cGMP). cGMP activates cGMP-dependent protein kinases (PRKGs), which can therefore be considered downstream effectors of NO signaling. Since NO is thought to be involved in the regulation of both sleep and circadian rhythms, we analyzed these two processes in mice deficient for cGMP-dependent protein kinase type I (PRKG1) in the brain. Prkg1 mutant mice showed a strikingly altered distribution of sleep and wakefulness over the 24 hours of a day as well as reductions in rapid-eye-movement sleep (REMS) duration and in non-REM sleep (NREMS) consolidation, and their ability to sustain waking episodes was compromised. Furthermore, they displayed a drastic decrease in electroencephalogram (EEG) power in the delta frequency range (1–4 Hz) under baseline conditions, which could be normalized after sleep deprivation. In line with the re-distribution of sleep and wakefulness, the analysis of wheel-running and drinking activity revealed more rest bouts during the activity phase and a higher percentage of daytime activity in mutant animals. No changes were observed in internal period length and phase-shifting properties of the circadian clock while chi-squared periodogram amplitude was significantly reduced, hinting at a less robust oscillator. These results indicate that PRKG1 might be involved in the stabilization and output strength of the circadian oscillator in mice. Moreover, PRKG1 deficiency results in an aberrant pattern, and consequently a reduced quality, of sleep and wakefulness, possibly due to a decreased wake-promoting output of the circadian system impinging upon sleep