It has been shown for the first time by transmission electron microscopy that the hydrated fullerene C60 inhibited the fibrillization of amyloid-beta25-35 peptide. The fullerene affected the amyloid-beta25-35 assembly, manifesting its anti-amyloidogenic capacity. Our in vivo investigations demonstrated also that a single intracerebroventricular injection of the C60 hydrated fullerene at a dose of 7.2 nmol/ventricle significantly improved the performance of the cognitive task in control rats. The intracerebroventricular injection of the C60 hydrated fullerene (3.6 nmol/ventricle) prevented the impairment of performance of the cognitive task induced by amyloid-beta25-35 (22.5 nmol/ventricle). The results obtained may be useful in the development of therapy of Alzheimer's disease.

The dynamics of the state of hippocampal pyramidal neurons after intrahippocampal microinjections of (1) amyloid-beta25-35 (1.6 nmol/1 microl), (2) an aqueous molecule-colloidal solution of C60 (0.46 nmol/1 microl) and (3) an aqueous molecule-colloidal solution of C60 before amyloid-beta25-35 administration were analysed in rats. This model allowed us to study the role of amyloid-beta25-35 in the pathogenesis of Alzheimer's disease and to test anti-amyloid substances. Methods of fluorescent (acridine orange) and brightfield (cresyl violet and immunohistochemistry) microscopy were used. Acridine orange staining indicated changes in protein synthesis intensity due to alterations in the rRNA state of neuron ribosomes. One day after administration of amyloid-beta25-35, the intensity of protein synthesis in the population of morphologically intact cells decreased by 45%. By day 14, degeneration occurred in the majority of pyramidal cells, and amyloid-beta25-35 deposits were observed in the neuronal cytoplasm. In necrotic cells, acridine orange staining of the cytoplasm was drastically increased as a result of RNA degradation rather than due to an increase in protein synthesis. Because amyloid-beta25-35 administration provoked oxidative stress, we assumed that an aqueous molecule-colloidal solution of C60 administered before amyloid-beta25-35 prevented protein synthesis changes on day 1, while acting as an antioxidant, and by day 14 it inhibited neurodegeneration and amyloid-beta25-35 accumulation. Based on the data that an aqueous molecule-colloidal solution of C60 prevented amyloid-beta25-35 aggregation in in vitro experiments and based on our present evidence on the antitoxicity of an aqueous molecule-colloidal solution of C60, we suggest that functionalised C60 prevents/diminishes amyloid-beta25-35 aggregation in vivo as well. Thus, an aqueous molecule-colloidal solution of C60 administered at a low concentration before amyloid-beta2-35, prevented disturbances in protein synthesis, neurodegeneration and formation amyloid-beta25-35 deposits in hippocampal pyramidal neurons in vivo. This evidence gives promise that functionalised C60 can be used to develop anti-amyloid drugs combining antioxidant and anti-aggregative properties.

Background Campylobacter is the main cause of bacterial gastroenteritis worldwide. The main transmission route is through consumption of food contaminated with Campylobacter species or contact with infected animals. In Latvia, the prevalence of campylobacteriosis is reported to be low (4.6 cases per 100,000 population in 2016). Aim To determine prevalence, species spectrum and antimicrobial resistance (AMR) of Campylobacter spp. in Latvia, using data from various livestock and human clinical samples. Methods We analysed data of Campylobacter microbiological monitoring and AMR (2008 and 2014–16) in Latvia. Data from broilers, poultry, pigs, calves and humans were used to determine prevalence of Campylobacter . Additionally, 45 different origin isolates (22 human) were sequenced on the Illumina MiSeq platform; for each isolate core genome multilocus sequence typing was used and relevant antimicrobial resistance mechanisms were identified. Results Overall, Campylobacter prevalence in was 83.3% in pigs, 50.2% in broilers, 16.1% in calves and 5.3% in humans; C. jejuni was the predominant species in all sources except pigs where C. coli was main species. High level of resistance in Campylobacter were observed against fluoroquinolones, tetracycline and streptomycin, in most of sequenced isolates genetic determinants of relevant AMR profiles were identified. Conclusions In Latvia, prevalence of Campylobacter in livestock is high, especially in pigs and broilers; prevalence in poultry and humans were lower than in other European countries. AMR analysis reveals increase of streptomycin and tetracycline resistant broiler origin C. jejuni strains. WGS demonstrates a high compliance between resistance phenotype and genotype for quinolones and tetracyclines.

We studied the effects of fullerene C60 nanoparticles, namely hydrated fullerene C60 (C60HyFn), on interrelations between EEG frequency spectra from the frontal cortex and the dorsal hippocampus (CA1) on an amyloid-β (Aβ) rat model of Alzheimer's disease (AD). Infusion of Aβ1-42 protein (1.5 μl) into the CA1 region two weeks before EEG testing diminished hippocampal theta (3.8-8.4 Hz) predominance and eliminated cortical beta (12.9-26.2 Hz) predominance observed in baseline EEG of rats infused with saline (control) or with C60HyFn alone. In contrast, these Aβ1-42 effects were abolished in rats pretreated with C60HyFn, 30 min apart. Dopaminergic mediation in AD has been shown to be involved in neuronal plasticity and Aβ transformation in different ways. To clarify its role in the cortex-hippocampus interplay in the Aβ model of AD, we used peripheral injection of a dopamine agonist, apomorphine (APO), at a low dose (0.1 mg/kg). In rats infused with C60HyFn or Aβ1-42 alone, APO attenuated the cortical beta predominance, with immediate and delayed phases evident in the Aβ1-42-rats. Pretreatment with C60HyFn diminished the APO effect in the Aβ1-42-treated rats. Thus, we show that intrahippocampal injection of Aβ1-42 dramatically disrupts cortical versus hippocampal EEG interrelations and that pretreatment with the fullerene eliminates this abnormality. We suggest that some effects of C60HyFn may be mediated through presynaptic dopamine receptors and that water-soluble C60 fullerenes have a neuroprotective potential.

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Background and Objectives: Legionella is one of the most important water-related pathogens. Inside the water supply systems and the biofilms, Legionella interact with other bacteria and free-living amoeba (FLA). Several amoebas may serve as hosts for bacteria in aquatic systems. This study aimed to investigate the co-occurrence of Legionella spp. and FLA in drinking water supply systems. Materials and Methods: A total of 268 water samples were collected from apartment buildings, hotels, and public buildings. Detection of Legionella spp. was performed in accordance with ISO 11731:2017 standard. Three different polymerase chain reaction (PCR) protocols were used to identify FLA. Results: Occurrence of Legionella varied from an average of 12.5% in cold water samples with the most frequent occurrence observed in hot water, in areas receiving untreated groundwater, where 54.0% of the samples were Legionella positive. The occurrence of FLA was significantly higher. On average, 77.2% of samples contained at least one genus of FLA and, depending on the type of sample, the occurrence of FLA could reach 95%. In the samples collected during the study, Legionella was always isolated along with FLA, no samples containing Legionella in the absence of FLA were observed. Conclusions: The data obtained in our study can help to focus on the extensive distribution, close interaction, and long-term persistence of Legionella and FLA. Lack of Legionella risk management plans and control procedures may promote further spread of Legionella in water supply systems. In addition, the high incidence of Legionella-related FLA suggests that traditional monitoring methods may not be sufficient for Legionella control.

Эозинофильный эзофагит-это хроническое иммунное антигенопосредованное воспалительное заболевание пищевода, характеризующееся выраженной эозинофильной инфильтрацией его слизистой оболочки. Повреждающее действие на слизистую оболочку пищевода оказывают генетическая предрасположенность и активация иммунологических реакций, опосредованных Т хелперами 2-го типа, а также воздействие пищевых и аэроаллергенов. В педиатрической практике эозинофильный эзофагит наиболее часто встречается у детей дошкольного и школьного возраста с отягощенным аллергологическим анамнезом. Клинически эозинофильный эзофагит выражается болью в эпигастрии, симптомами, сходными с гастроэзофагеальной рефлюксной болезнью, дисфагией. Диагностика эозинофильного эзофагита основывается на клинической симптоматике, характерных эндоскопических и морфологических изменениях слизистой оболочки пищевода. В статье приведены алгоритмы обследования, динамического наблюдения и лечения детей с эозинофильным эзофагитом, разработанные Европейским обществом детских гастроэнтерологов, гепатологов и нутрициологов (ESPGHAN); описана технология взятия биоптатов слизистой оболочки пищевода при подозрении на эозинофильный эзофагит. Лечение детей с эозинофильным эзофагитом базируется на следующих подходах: пробное лечение ингибиторами протонной помпы в течение 2 мес, диетическая коррекция и, при неэффективности, применение топических глюкокортикостероидов.

ВВЕДЕНИЕРост распространенности пищевой аллергии, в том числе у детей, делает эту форму патологии все более актуальной проблемой педиатрии [1,2].Согласно определению, пищевая аллергия -это пато-логическая реакция на компоненты пищи, в основе которой лежат иммунные механизмы, включая выработку специфи-ческих иммуноглобулинов (Immunoglobulin, Ig) E (IgE-опо-сре дованные аллергические реакции), клеточный иммун-ный ответ (не-IgE-опосредованные аллергические реакции) и сочетание этих двух механизмов (реакции смешанного типа -IgE-опо средованные и не-IgE-опосредованные) [1]. При этом не-IgE-опосредованные аллергические реакции на пищу, особенно изолированные гастроинтестинальные проявления аллергии при отсутствии кожных высыпаний, вызывают наибольшие трудности в диагностике.Целью настоящего обзора является ознакомление педиатров с современными представлениями о патогенезе гастроинтестинальной пищевой аллергии и с актуальными принципами ее диагностики.