РЕНАЛЬНА ЕРИТРОПОЕТИНДЕФІЦИТНА АНЕМІЯ У ВАГІТНИХ ЖІНОК З ІНФЕКЦІЙНИМИ УРАЖЕННЯМИ НИРОК

A level of erythropoietin was determined in the group of pregnante women with such illnesses as chronic pyelonephritis, keen pyelonephritis and in healthy women with 28-40 weeks of pregnancy. The group of pregnant woman with urinary tract infections are distributed by the level of haemoglobin in the blood. We found interesting results in the group of chronic pyelonephritis and anemia on the middle stage. By means of this research we came at a conclusion that the level of erythropoietin should be determined in the blood serum in women with urinary tract infections and anemia on the middle or grave stage in order to solve the question of chosing the way of treatment in such women.Определялся уровень эритропоэтина у беременных женщин в группах с острым пиелонефритом, с хроническим пиелонефритом и у контрольной группе (здоровые беременные) в сроках от 28 до 40 недель беременности. Группы беременных с воспалительными заболеваниями почек распределены по уровню гемоглобина в крови. Интересные результаты получены в группе с хроническим пиелонефритом и анемией средней степени: у 3(4,8%) беременных уровень эритропоэтина был в нижних границах нормы и у 20 (32,3%) женщин выше нормы, а у большенства у несколько раз. На основании данного исследования рекомендуется беременным женщинам с воспалительным и заболеваниями почек и анемией средней и тяжелой степени определятьуровень эритропоэтина в сыворотке крови, для решения вопроса о выборе метода леченияВизначався рівень еритропоетину в крові вагітних жінок з інфекційними ураженнями нирок. Обстежувані вагітні розподілені на три групи: гострий пієлонефрит, хронічний пієлонефрит та здорові вагітні (контрольна група). Всі вагітні були втермінах між 28 та 40 тижнем вагітності. Групи вагітних з запальними ураженнями нирок розподілені за рівнем гемоглобіну в крові ще на три групи: анемія легкого ступеня, середнього ступеня та важка анемія. Цікаві результати отримали в групі вагітних з хронічним пієлонефритом та анемією середнього ступеня: у 3 (4,8%) вагітних рівень еритропоетину був в нижніх межах норми, у 20 (32,3%) вагітних вище норми, а у більшості вище норми в де кілька разів. Виходячи з даного дослідження, рекомендуємо вагітним жінкам з запальними захворюваннями нирок та анемією середнього та важкого ступеня визначати рівень еритропоетину в сироватці крові, для вирішення питання про метод лікування анемі у таких вагітних жінок

Clinical and experimental comparisons of fetal alcohol syndrome

The adverse effects of alcohol on the developing human represent a spectrum of structural anomalies and behavioral and neurocognitive disabilities, most accurately termed fetal alcohol spectrum disorders (FASD). In animal models of FASD, ethanol causes a number of changes in brain development, with many of these changes being very transient. In the same number it is necessary to carry experimental works: to estimate intra-uterine influence of alcohol on development structures of the central excitatory system at experimental animals. Researches on rats of line Vistar. Anim als received instead of water within a month up to pregnancy and during all pregnancy of 15 % a solution of spirit. From the received posterity in the age of one month for optical research took a brain of a bark of a touch zone, hypothalamic areas and a cerebellum. Except for that for 9-12 day of pregnancy defined a level of the transforming factor of growth beta one (TGF-β1) at animals of the given experiment. At animals developmental anomalies of eyes, ears, and skulls were observed. The expressed changes have been found. Dystrophic changes neurons have been expressed. Comparing obtained data with parameters TGF- β1, we had noted been increase of concentration in skilled group. Thus, revealed features TGF- β1 are comparable to morphological changes in a brain, can be conditionally connected on sim ilar by the processes, arising mammals and the person.Данная статья посвящена клинико-экспериметальным сопоставлениям антенатального воздействия алкоголя на центральную нервную систему развивающегося организма ребенка. С этой целью нами проведен эксперимент на крысах стадного разведения линии Вистар, алкоголизированных в течение месяца до беременности и во время беременности. У полученного потомства в возрасте одного месяца для светооптического исследования брали головной мозг. Также проанализирован уровень трансформирующего фактора роста 01 (TGF- β1) у животных во время беременности с использованием метода гетерогенного твердофазного иммуноферментного анализа

USP18-Based Negative Feedback Control Is Induced by Type I and Type III Interferons and Specifically Inactivates Interferon α Response

Type I interferons (IFN) are cytokines that are rapidly secreted upon microbial infections and regulate all aspects of the immune response. In humans 15 type I IFN subtypes exist, of which IFN α2 and IFN β are used in the clinic for treatment of different pathologies. IFN α2 and IFN β are non redundant in their expression and in their potency to exert specific bioactivities. The more recently identified type III IFNs (3 IFN λ or IL-28/IL-29) bind an unrelated cell-type restricted receptor. Downstream of these two receptor complexes is a shared Jak/Stat pathway. Several mechanisms that contribute to the shut down of the IFN-induced signaling have been described at the molecular level. In particular, it has long been known that type I IFN induces the establishment of a desensitized state. In this work we asked how the IFN-induced desensitization integrates into the network built by the multiple type I IFN subtypes and type III IFNs. We show that priming of cells with either type I IFN or type III IFN interferes with the cell's ability to further respond to all IFN α subtypes. Importantly, primed cells are differentially desensitized in that they retain sensitivity to IFN β. We show that USP18 is necessary and sufficient to induce differential desensitization, by impairing the formation of functional binding sites for IFN α2. Our data highlight a new type of differential between IFNs α and IFN β and underline a cross-talk between type I and type III IFN. This cross-talk could shed light on the reported genetic variation in the IFN λ loci, which has been associated with persistence of hepatitis C virus and patient's response to IFN α2 therapy

ISG15 Is Critical in the Control of Chikungunya Virus Infection Independent of UbE1L Mediated Conjugation

Chikungunya virus (CHIKV) is a re-emerging alphavirus that has caused significant disease in the Indian Ocean region since 2005. During this outbreak, in addition to fever, rash and arthritis, severe cases of CHIKV infection have been observed in infants. Challenging the notion that the innate immune response in infants is immature or defective, we demonstrate that both human infants and neonatal mice generate a robust type I interferon (IFN) response during CHIKV infection that contributes to, but is insufficient for, the complete control of infection. To characterize the mechanism by which type I IFNs control CHIKV infection, we evaluated the role of ISG15 and defined it as a central player in the host response, as neonatal mice lacking ISG15 were profoundly susceptible to CHIKV infection. Surprisingly, UbE1L−/− mice, which lack the ISG15 E1 enzyme and therefore are unable to form ISG15 conjugates, displayed no increase in lethality following CHIKV infection, thus pointing to a non-classical role for ISG15. No differences in viral loads were observed between wild-type (WT) and ISG15−/− mice, however, a dramatic increase in proinflammatory cytokines and chemokines was observed in ISG15−/− mice, suggesting that the innate immune response to CHIKV contributes to their lethality. This study provides new insight into the control of CHIKV infection, and establishes a new model for how ISG15 functions as an immunomodulatory molecule in the blunting of potentially pathologic levels of innate effector molecules during the host response to viral infection

Transcription analysis on response of swine lung to H1N1 swine influenza virus

<p>Abstract</p> <p>Background</p> <p>As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore it, a time-course gene expression profiling was performed for comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs.</p> <p>Results</p> <p>At the early stage of H1N1 swine virus infection, pigs were suffering mild respiratory symptoms and pathological changes. A total of 268 porcine genes showing differential expression (DE) after inoculation were identified to compare with the controls on day 3 post infection (PID) (Fold change ≥ 2, p < 0.05). The DE genes were involved in many vital functional classes, mainly including signal transduction, immune response, inflammatory response, cell adhesion and cell-cell signalling. Noticeably, the genes associated with immune and inflammatory response showed highly overexpressed. Through the pathway analysis, the significant pathways mainly concerned with Cell adhesion molecules, Cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway and MAPK signaling pathway, suggesting that the host took different strategies to activate these pathways so as to prevent virus infections at the early stage. However, on PID 7, the predominant function classes of DE genes included signal transduction, metabolism, transcription, development and transport. Furthermore, the most significant pathways switched to PPAR signaling pathway and complement and coagulation cascades, showing that the host might start to repair excessive tissue damage by anti-inflammatory functions. These results on PID 7 demonstrated beneficial turnover for host to prevent excessive inflammatory damage and recover the normal state by activating these clusters of genes.</p> <p>Conclusions</p> <p>This study shows how the target organ responds to H1N1 swine influenza virus infection in pigs. The observed gene expression profile could help to screen the potential host agents for reducing the prevalence of swine influenza virus and further understand the molecular pathogenesis associated with H1N1 infection in pigs.</p

Activation of Human Monocytes by Live Borrelia burgdorferi Generates TLR2-Dependent and -Independent Responses Which Include Induction of IFN-β

It is widely believed that innate immune responses to Borrelia burgdorferi (Bb) are primarily triggered by the spirochete's outer membrane lipoproteins signaling through cell surface TLR1/2. We recently challenged this notion by demonstrating that phagocytosis of live Bb by peripheral blood mononuclear cells (PBMCs) elicited greater production of proinflammatory cytokines than did equivalent bacterial lysates. Using whole genome microarrays, we show herein that, compared to lysates, live spirochetes elicited a more intense and much broader transcriptional response involving genes associated with diverse cellular processes; among these were IFN-β and a number of interferon-stimulated genes (ISGs), which are not known to result from TLR2 signaling. Using isolated monocytes, we demonstrated that cell activation signals elicited by live Bb result from cell surface interactions and uptake and degradation of organisms within phagosomes. As with PBCMs, live Bb induced markedly greater transcription and secretion of TNF-α, IL-6, IL-10 and IL-1β in monocytes than did lysates. Secreted IL-18, which, like IL-1β, also requires cleavage by activated caspase-1, was generated only in response to live Bb. Pro-inflammatory cytokine production by TLR2-deficient murine macrophages was only moderately diminished in response to live Bb but was drastically impaired against lysates; TLR2 deficiency had no significant effect on uptake and degradation of spirochetes. As with PBMCs, live Bb was a much more potent inducer of IFN-β and ISGs in isolated monocytes than were lysates or a synthetic TLR2 agonist. Collectively, our results indicate that the enhanced innate immune responses of monocytes following phagocytosis of live Bb have both TLR2-dependent and -independent components and that the latter induce transcription of type I IFNs and ISGs