AWARENESS OF LYME BORRELIOSIS OF THE PATIENTS OF TERNOPIL REGIONAL TB DISPENSARY

Background. Lyme disease has many clinical features similar tothose in sarcoidosis and tuberculosis. Epidemiological data in the world, in particular in Ukraine, proves the increase in Lyme borreliosis incidence. Ternopil region is endemic with Lyme borreliosis.Objective. The research was aimed to investigate the prevalence of infection with Borrelia burgdorferi and epidemiology features of borreliosis among the patients of Ternopil Regional TB Dispensary.Methods. In total, 29 patients were admitted to Departments of Differential Diagnostic, TB Therapy and TB Surgery of Ternopil Regional TB Dispensary in October 2016-January 2017. All the surveyed answered the questions of an integrated international questionnaire, where they noted the area and a number of tick bites, described the removal method, noted the survey for borreliosis pathogen and complaints after tick bites.Results. It was established that 5 respondents had a history of tick bites episodes, but only in one case the patient was examined of borreliosis. Tick bites were noticed in 3 patients with sarcoidosis and 1 with tuberculosis (TB) and exudative pleurisy, respectively.Conclusions. The absence of appeals for medical care, lack of sufficient information on Lyme borreliosis and disuse of preventive measures for tick bites by the interviewed patients of Ternopil regional TB dispensary departments proves the need of improvement of health education on Lyme borreliosis (LB) among this category of population. 24 (82.7%) of 29 respondents did not remember the tick bite. The symptoms of (LB) are similar to those in sarcoidosis and tuberculosis (pleural lesions, heart, joints, nervous system, skin), and the presence of tick bites gives the reasons to examine these patients of Borrelia burgdorferi senso lato

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.

Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2(V617F) Mice

Rationale: The mechanisms driving atherothrombotic risk in individuals with JAK2(V617F) (Jak2(VF)) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood. Objective: The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2(VF) expression. Methods and Results: Irradiated low-density lipoprotein receptor knockout (Ldlr(-/-)) mice were transplanted with bone marrow from wild-type or Jak2(VF) mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2(VF) mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2(VF) lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2(VF) erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a "don't-eat-me" signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2(VF) macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis. Conclusions: Hematopoietic Jak2(VF) expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2(VF) caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability

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

Clinical use of amyloid-positron emission tomography neuroimaging: Practical and bioethical considerations

Until recently, estimation of β-amyloid plaque density as a key element for identifying Alzheimer's disease (AD) pathology as the cause of cognitive impairment was only possible at autopsy. Now with amyloid-positron emission tomography (amyloid-PET) neuroimaging, this AD hallmark can be detected antemortem. Practitioners and patients need to better understand potential diagnostic benefits and limitations of amyloid-PET and the complex practical, ethical, and social implications surrounding this new technology. To complement the practical considerations, Eli Lilly and Company sponsored a Bioethics Advisory Board to discuss ethical issues that might arise from clinical use of amyloid-PET neuroimaging with patients being evaluated for causes of cognitive decline. To best address the multifaceted issues associated with amyloid-PET neuroimaging, we recommend this technology be used only by experienced imaging and treating physicians in appropriately selected patients and only in the context of a comprehensive clinical evaluation with adequate explanations before and after the scan

Hybrid- and complex-type N-glycans are not essential for Newcastle disease virus infection and fusion of host cells

N-linked glycans are composed of three major types: high-mannose (Man), hybrid or complex. The functional role of hybrid- and complex-type N-glycans in Newcastle disease virus (NDV) infection and fusion was examined in N-acetylglucosaminyltransferase I (GnT I)-deficient Lec1 cells, a mutant Chinese hamster ovary (CHO) cell incapable of synthesizing hybrid- and complex-type N-glycans. We used recombinant NDV expressing green fluorescence protein or red fluorescence protein to monitor NDV infection, syncytium formation and viral yield. Flow cytometry showed that CHO-K1 and Lec1 cells had essentially the same degree of NDV infection. In contrast, Lec2 cells were found to be resistant to NDV infection. Compared with CHO-K1 cells, Lec1 cells were shown to more sensitive to fusion induced by NDV. Viral attachment was found to be comparable in both lines. We found that there were no significant differences in the yield of progeny virus produced by both CHO-K1 and Lec1 cells. Quantitative analysis revealed that NDV infection and fusion in Lec1 cells were also inhibited by treatment with sialidase. Pretreatment of Lec1 cells with Galanthus nivalis agglutinin specific for terminal α1-3-linked Man prior to inoculation with NDV rendered Lec1 cells less sensitive to cell-to-cell fusion compared with mock-treated Lec1 cells. Treatment of CHO-K1 and Lec1 cells with tunicamycin, an inhibitor of N-glycosylation, significantly blocked fusion and infection. In conclusion, our results suggest that hybrid- and complex-type N-glycans are not required for NDV infection and fusion. We propose that high-Man-type N-glycans could play an important role in the cell-to-cell fusion induced by NDV

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012