Palaeoclimate evidence of vulnerable permafrost during times of low sea ice.

Climate change in the Arctic is occurring rapidly, and projections suggest the complete loss of summer sea ice by the middle of this century1. The sensitivity of permanently frozen ground (permafrost) in the Northern Hemisphere to warming is less clear, and its long-term trends are harder to monitor than those of sea ice. Here we use palaeoclimate data to show that Siberian permafrost is robust to warming when Arctic sea ice is present, but vulnerable when it is absent. Uranium-lead chronology of carbonate deposits (speleothems) in a Siberian cave located at the southern edge of continuous permafrost reveals periods in which the overlying ground was not permanently frozen. The speleothem record starts 1.5 million years ago (Ma), a time when greater equator-to-pole heat transport led to a warmer Northern Hemisphere2. The growth of the speleothems indicates that permafrost at the cave site was absent at that time, becoming more frequent from about 1.35 Ma, as the Northern Hemisphere cooled, and permanent after about 0.4 Ma. This history mirrors that of year-round sea ice in the Arctic Ocean, which was largely absent before about 0.4 Ma (ref. 3), but continuously present since that date. The robustness of permafrost when sea ice is present, as well as the increased permafrost vulnerability when sea ice is absent, can be explained by changes in both heat and moisture transport. Reduced sea ice may contribute to warming of Arctic air4-6, which can lead to warming far inland7. Open Arctic waters also increase the source of moisture and increase autumn snowfall over Siberia, insulating the ground from low winter temperatures8-10. These processes explain the relationship between an ice-free Arctic and permafrost thawing before 0.4 Ma. If these processes continue during modern climate change, future loss of summer Arctic sea ice will accelerate the thawing of Siberian permafrost.

[Immunohistochemical detection of biomolecular markers for metaplastic mucosal atrophy in gastric biopsy specimens].

OBJECTIVE: To estimate the validity of the signs of metaplastic atrophic gastritis to elaborate a marker principle of its detection. SUBJECTS AND METHODS: Two hundred diagnostic cases morphologically diagnosed with chronic gastritis were selected for examination. The validity of the histological and immunohistochemical signs/markers reflecting a gland abnormality (hyperplasia of smooth muscle cells and argyrophilic and elastic fibers) and a cell phenotype change (intestinal and pyloric metaplasia): CDX-2, Shh, villin, CD10, MUC2, and MUC5AC was estimated in gastric biopsy specimens with atrophic gastritis forms verified in accordance with international classifications. The validity of the signs/markers was assessed, by calculating the sensitivity, specificity, prognostic value of positive and negative results, and positive and negative likelihood ratios. RESULTS: There were 3 molecules: CDX-2 is a nuclear transcription factor associated with intestinal differentiation; CCD10 is a brush border membrane-bound mycin and MUC2 is an intestinal-type mycin, which showed a high validity like the markers of metaplastic atrophic gastritis. An algorithm that could probably evaluate atrophic gastritis was elaborated for the successive immunohistochemical identification of the above-mentioned marker. CONCLUSION: The proposed technical decision to verify atrophic gastritis by the biomarker method may be not an alternative, but complementary technique of identifying the form of atrophic gastritis.

Strong coupling between a microwave photon and a singlet-triplet qubit.

Combining superconducting resonators and quantum dots has triggered tremendous progress in quantum information, however, attempts at coupling a resonator to even charge parity spin qubits have resulted only in weak spin-photon coupling. Here, we integrate a zincblende InAs nanowire double quantum dot with strong spin-orbit interaction in a magnetic-field resilient, high-quality resonator. The quantum confinement in the nanowire is achieved using deterministically grown wurtzite tunnel barriers. Our experiments on even charge parity states and at large magnetic fields, allow us to identify the relevant spin states and to measure the spin decoherence rates and spin-photon coupling strengths. We find an anti-crossing between the resonator mode in the single photon limit and a singlet-triplet qubit with a spin-photon coupling strength of g/2π = 139 ± 4 MHz. This coherent coupling exceeds the resonator decay rate κ/2π = 19.8 ± 0.2 MHz and the qubit dephasing rate γ/2π = 116 ± 7 MHz, putting our system in the strong coupling regime.

Experimental evaluation of speckle suppression efficiency using a moving 2D Barker code DOE.

This paper reports the findings from an experimental evaluation of speckle suppression efficiency using a method based on a moving 2D Barker code diffractive optical element (DOE). The optical setup and the optical scheme parameters of the method are presented. A speckle contrast of ~4.4-5.3% and speckle suppression coefficient (coefficient of speckle contrast reduction) of k>8 was obtained in experiments. However, the experimentally obtained speckle suppression coefficient was approximately 1.5 times smaller than the theoretical prediction. It is speculated that the discrepancy between the theoretical and the experimental data is due to an inexact match between the optical setup and the optimal optical parameters of the method. Analysis of the experimental data revealed that once the optical scheme is optimized, it will be possible to obtain a speckle suppression that is closer to the theoretical prediction.

Optical schemes for speckle suppression by Barker code diffractive optical elements.

A method for speckle suppression based on Barker code and M-sequence code diffractive optical elements (DOEs) is analyzed. An analytical formula for the dependence of speckle contrast on the wavelength of the laser illumination is derived. It is shown that speckle contrast has a wide maximum around the optimal wavelength that makes it possible to obtain large speckle suppression by using only one DOE for red, green, and blue laser illumination. Optical schemes for implementing this method are analyzed. It is shown that the method can use a simple liquid-crystal panel for phase rotation instead of a moving DOE; however, this approach requires a high frequency of liquid-crystal switching. A simple optical scheme is proposed using a 1D Barker code DOE and a simple 1D liquid-crystal panel, which does not require a high frequency of liquid-crystal switching or high-accuracy DOE movement.

Performance of high impedance resonators in dirty dielectric environments.

High-impedance resonators are a promising contender for realizing long-distance entangling gates between spin qubits. Often, the fabrication of spin qubits relies on the use of gate dielectrics which are detrimental to the quality of the resonator. Here, we investigate loss mechanisms of high-impedance NbTiN resonators in the vicinity of thermally grown SiO2 and Al2O3 fabricated by atomic layer deposition. We benchmark the resonator performance in elevated magnetic fields and at elevated temperatures and find that the internal quality factors are limited by the coupling between the resonator and two-level systems of the employed oxides. Nonetheless, the internal quality factors of high-impedance resonators exceed 103 in all investigated oxide configurations which implies that the dielectric configuration would not limit the performance of resonators integrated in a spin-qubit device. Because these oxides are commonly used for spin qubit device fabrication, our results allow for straightforward integration of high-impedance resonators into spin-based quantum processors. Hence, these experiments pave the way for large-scale, spin-based quantum computers.

[A method for the detection and characterization of GABA(A) receptors by calcium-sensitive fluorescent probes].

A method for the detection and characterization of GABA(A) receptors of neurons has been developed, which is based on the measurement of the activity of potential-dependent calcium channels using the fluorescence of the two-wavelength calcium-sensitive probe Fura-2. The method makes it possible to detect the ligands of GABA(A) receptors and determine the constants of activation and inhibition as well as the type of inhibition. The object of investigation was a young (two- to four-day-old) rat hippocampal cell culture in which GABA induces the depolarization and a transient increase in Ca2+ concentration in the cytosol of neurons due to the activation of potential-dependent calcium channels. It was shown that a short-time application of GABA induces a decrease in the amplitude of calcium responses to subsequent addition of the depolarizing agents GABA or KCl. However, at low amplitudes of calcium responses to the addition of GABA, this reducing effect on the subsequent addition of KCl was insignificant. It was found that the amplitudes of calcium responses to KCl and GABA are linearly dependent on the angular coefficient b = 3.41. This enabled one to develop a method of normalizing calcium signals, which makes it possible to compare experiments performed on different days and different cultures. By using this normalization technique, the values of EC50 = 2.21 +/- 0.14 ?M and the Hill coefficient = 1.9 +/- 0.2 were estimated. The blocker of potential-dependent calcium channels nifedipine suppressed simultaneously the amplitudes of calcium responses to the addition of KCl and GABA. In this case, the linear relationship between the amplitudes of calcium responses to the addition of KCl and GABA was retained. To verify the validity of the method, the constant of inhibition of a calcium signal and the type of inhibition for known noncompetitive and competitive antagonists of GABA(A) receptors were determined.

[Reactive changes of human gastric mucosa infected with Helicobacter pylori in the aspect of genetic characteristic of host inflammatory response].

The aim of this study was to determine the morphological changes of human gastric mucosa infected with Helicobacter pylori (HP) depending on polymorphism of the genes coding both interleukin-1beta and interleukin-1 receptor antagonist. 106 juveniles with HP-induced chronic gastritis were studied along with 44 juveniles with gastritis, not associated with HP. In patients with HP-associated gastritis, the significant increase in epithelial proliferation and apoptosis indexes was observed. Epithelium proliferation zone was expanded in the direction of surface foveolar epithelium and into the depth of glands; pronounced lympho-plasma cell infiltration of mucosal lamina propria was observed. Cytokine gene polymorphisms were evaluated by PCR. The results suggest an association between more pronounced inflammation of gastric mucosa with the T allele of interleukin-1beta C -511 C > T gene polymorphous locus (Chi2 = 14.006; p = 0.001). No association was found of the interleukin-1beta C +3953 T gene and the variable number of tandem repeats in the 2nd introne of interleukin 1 receptor antagonist gene with morphological changes in the gastric mucosa.

[Morphogenesis of gastric mucosal atrophy as a basis of a phenotype of chronic gastritis].

Atrophic antral gastritis was found to show an absolute decrease in gland volume with higher expression of the gastric transcription factor Shh, i.e. absolute atrophy and that concurrent with the replacement of the specialized gastric epithelium by the intestinal MUC2-producing one, i.e. metaplastic atrophy. In atrophic multifocal gastritis along absolute and metaplastic atrophy, there are foci of the proliferative metaplastic epithelium, i.e. hyperproliferative metaplastic atrophy that is prevalent in atrophic pangastritis. The molecular characteristics of hyperproliferative metaplastic atrophy are varying: in some foci of metaplasia, the high proliferative activity of the epithelium is concomitant with the hyperexpression of P53, a marker of DNA damage, the lower expression of the intestinal transcription factor CDX-2, and the low level of Cpp32, an indicator of apoptosis. Whether such structures can be identified at the launching pad for tumor growth in atrophic pangastritis is discussed.

[The Russian revision of chronic gastritis classification: reproducibility of the pathomorphologic picture].

The estimation of Russian revision reproducibility of the chronic gastritis OLGA system International classification has been spent. The analysis of Russian pathologists-experts work, considered in estimations of an expression level and prevalence of gastric mucosal atrophic changes, as a tumour predictor, for the identification of chronic gastritis stages (0-IV) has been carried out by kappa-statistics. The different levels of experts' consent according to consent criteria calculation have been estimated. The criteria of consent (k) of leading Russian pathologists have been 0.5 (moderate level of the agreement). In the practice of histopathology researchers' classification a consent level has been lower--from 0.27 (satisfactory or tolerable consent level) to 0.42 (moderate or average consent level). A subjective reasons reducing consistency level of pathologists-experts have been discussed.

[Proliferative and mucin-producing activities in the foci of intestinal metaplasia associated with chronic atrophic gastritis and gastric ulcer].

Immunohistochemical studies revealed the dependence of cell regeneration parameters at sites of intestinal metaplasia (IM) in gastric mucosa (GM) on the character of the background events, such as atrophy and erosive-ulcerative defect. Mucin profile was determined in various types of IM. The intestinal type of mucin was found only in type I IM while types II and III were characterized by the mixed gastrointestinal phenotype with expression MUCSAC and MUC2. It was shown that at sites of incomplete IM (types II and III) and atrophic changes of GM cells proliferation activity of epithelium is considerably increased; this increase may be associated with the risk of developing gastric cancer of the intestinal type.

[Polymorphism of cytokine genes in the development of Helicobacter pylori infection].

The purpose of this work was to study morphological features of gastric mucosa depending on polymorphism of IL-l1beta and IL-1RN genes in children with chronic gastritis infected with different strains of Helicobacter pylori 0. We examined 106 children with HP-associated gastritis. The results suggest association of mucosal inflammation with T allele in polymorphous C-511T locus of IL-1beta (beta2 = 14,006; alpha = 0.001). agA + strains of HP were more frequently identified in patients with erosive ulcerative defects of gastric mucosa than in children with superficial gastritis (p < 0.05). The possibility of gene typing to form a group of patients with the unfavourable post-eradication clinical course for the prevention of duodenal ulcer and stomach cancer is discussed.

[Case of disseminated intestinal and cutaneous thromboangiitis (Kohlmeier-Degos' syndrome)].

Disseminated intestinal and cutaneous thromboangiitis (Kohlmeier-Degos' syndrome) is a rare syndrome of unknown etiology, which is characterized by cutaneous and visceral involvement. Two (cutaneous and visceral) stages are identified. A fatal outcome is inevitable although there may be a long (8-20-year) course of the disease during a benign process. The causes of death are peritonitis, central nervous system impairments, pleurisy, pericarditis. The paper describes a case of disseminated intestinal and cutaneous thromboangiitis (Kohlmeier-Degos' syndrome) in a 32-year-old female patient who has died from intoxication due to severely impaired permeability of the epithelial barrier mainly of the large bowel (diphtheritic inflammation of the mucosa, severe inflammatory edema of the submucous layer, and fibrinous impregnation of the serous membrane).

[Genetic regulation and phenotype of inflammation in Helicobacter pylori infection].

The problem of the relationships between the macro- and microorganism in Helicobacter pylori infection is discussed in the context of the genetic regulation of inflammation. The leading role of host genetic polymorphism in maintaining an inflammatory response in the absence of the infectious organism is demonstrated, by using previous Helicobacter gastritis as an example. The combinations of polymorphisms of two genes IL-1beta-511T/IL-1RN . 2 and IL-1beta-31T/IL-1RN . 2, which provides an inflammation phenotype associated with the risk of impaired cell renewal and gastric mucosal atrophy, have been identified. The promising use of the phenotype of chronic atrophic gastritis in the present classifications as a prognostic category of gastric cancer is assessed.

[International classification of chronic gastritis: what should be taken and what is in doubt].

The authors review the used classifications of chronic gastritis: Modified Sydney system, Atrophy Club classification, and Operative Link for Gastritis Assessment (OLGA). Their concept apparatus: the grade and stage of gastritis, intestinal metaplasia as a marker of gastric mucosal athrophy is considered. The possibilities of interpreting the pathologist's report and clinicomorphological comparisons are discussed. The OLGA Classification, which is to predict the gastric cancer risk determined by the degree of mucosal atrophy (a stage of chronic gastritis), is noted to have an indubitable merit. A simplified classification, according to which the grade and stage of gastritis are determined by the modified visual analog scale for mucosal changes in the body of the stomach and its antral part, is proposed. Whether the postmortem study protocol for gastric biopsy specimens can be modified is discussed.

[New methodology for the stabilometric diagnosis of equilibrium dysfunction].

The necessity of studying the dynamic stabilization of the human body vertical position is substantiated. New capacities of a stabilometric vector analysis in diagnosing equilibrium dysfunction, evaluating the efficiency of treatment, and determining the statistical significance of differences in the results in a patient rather than in a group of subjects are shown.

Transmission of lumpy skin disease virus: A short review.

Lumpy skin disease (LSD) is a viral transboundary disease endemic throughout Africa and of high economic importance that affects cattle and domestic water buffaloes. Since 2012, the disease has spread rapidly and widely throughout the Middle Eastern and Balkan regions, southern Caucasus and parts of the Russian Federation. Before vaccination campaigns took their full effect, the disease continued spreading from region to region, mainly showing seasonal patterns despite implementing control and eradication measures. The disease is capable of appearing several hundred kilometers away from initial (focal) outbreak sites within a short time period. These incursions have triggered a long-awaited renewed scientific interest in LSD resulting in the initiation of novel research into broad aspects of the disease, including epidemiology, modes of transmission and associated risk factors. Long-distance dispersal of LSDV seems to occur via the movement of infected animals, but distinct seasonal patterns indicate that arthropod-borne transmission is most likely responsible for the swift and aggressive short-distance spread of the disease. Elucidating the mechanisms of transmission of LSDV will enable the development of more targeted and effective actions for containment and eradication of the virus. The mode of vector-borne transmission of the disease is most likely mechanical, but there is no clear-cut evidence to confirm or disprove this assumption. To date, the most likely vectors for LSDV transmission are blood-sucking arthropods such as stable flies (Stomoxys calcitrans), mosquitoes (Aedes aegypti), and hard ticks (Rhipicephalus and Amblyomma species). New evidence suggests that the ubiquitous, synanthropic house fly, Musca domestica, may also play a role in LSDV transmission, but this has not yet been tested in a clinical setting. The aim of this review is to compile and discuss the earlier as well as the most recent research data on the transmission of LSDV.

Determination of lumpy skin disease virus in bovine meat and offal products following experimental infection.

Lumpy skin disease (LSD) has recently expanded its range northwards to include the Balkans, Turkey and Russia. Because there was no solid evidence conclusively verifying the transmission mechanism in the field and LSDV viraemic animals with overt and asymptomatic presentation of disease and their products may represent a risk as an indirect transmission pathway. In this work, we used PCR positivity and infectivity in clinical and subclinical infection to evaluate the safety of meat and offal products from cows infected with the virulent LSDV strain Russia/Dagestan/2015. At day 21 post infection, seven of the 12 animals developed the generalized disease, and four animals became subclinically infected without apparent clinical signs. Upon examination and necropsy, the animals with the generalized disease had skin lesions; noticeably enlarged lymph nodes; and lesions in the lungs, trachea and testicles; whereas subclinically ill animals exhibited only enlarged lymph nodes and fever. For both disease presentations, testing of skeletal meat by PCR and virus isolation showed that the skeletal meat did not contain live virus or viral genome, whereas in cattle with generalized disease, meat with gross pathology physically connected under the site of a skin lesion was positive for the live virus. In subclinical infection, only enlarged lymph nodes carried the infectious virus, while the other internal organs tested in both types of disease manifestation were negative except for the testicles. Overall, our findings demonstrate that clinically and subclinically infected animals are reservoirs of live LSDV in lymph nodes and testicles, whereas deep skeletal meat in both types of infection do not carry live virus and the risk of transmission through this product seems very low. The detection of LSDV in testicular tissues in subclinically ill animals is concerning because of the potential to spread infection through contaminated semen. This aspect requires reconsideration of surveillance programmes to identify these Trojan horses of LSDV infection.

Detection of vaccine-like lumpy skin disease virus in cattle and Musca domestica L. flies in an outbreak of lumpy skin disease in Russia in 2017.

Since 2012, lumpy skin disease virus (LSDV) has been spreading from the Middle East to south-east Europe and Russia. Although vaccination campaigns have managed to contain LSDV outbreaks, the risk of further spread is still high. The most likely route of LSDV transmission in short distance spread is vector-borne. Several arthropod species have been suggested as potential vectors, but no proven vector has yet been identified. To check whether promiscuous-landing synanthropic flies such as the common housefly (Musca domestica) could be involved, we carried out entomological trapping at the site of a recent LSDV outbreak caused by a vaccine-like LSDV strain. The presence of vaccine-like LSDV DNA was confirmed by the assay developed herein, the assay by Agianniotaki et al. (2017) and RPO30 gene sequencing. No evidence of field LSDV strain circulation was revealed. In this study, we discovered that M. domestica flies carried vaccine-like LSDV DNA (Ct  > 25.5), whereas trapped stable flies from the same collection were negative for both field and vaccine LSDV. To check whether flies were contaminated internally and externally, 50 randomly selected flies from the same collection were washed four times and tested. Viral DNA was mainly detected in the 1st wash fluid, suggesting genome or even viral contamination on the insect cadaver. In this study, internal contamination in the insect bodies without differentiation between the body locations was also revealed; however, the clinical relevance for mechanical transmission is unknown. Further work is needed to clarify a role of M. domestica in the transmission of LSDV. To our knowledge, this is the first report demonstrating that an attenuated LSD vaccine strain has been identified in Russian cattle given the ban on the use of live attenuated vaccines against LSDV.

Epidemiological characterization of lumpy skin disease outbreaks in Russia in 2016.

In 2015, the lumpy skin disease virus spread throughout the Russian Federation. Following a modified stamping-out campaign, the disease re-emerged with a greater incidence across 16 regions of Southern and Central Russia. A total of 313 outbreaks were reported to OIE. The highest outbreak frequency was observed in the republics of Chechnya (108), Kalmykiya (57), and Ingushetiya (35). The disease cases predominantly occurred in June and July 2016, starting from May to December; however, no association between outbreaks and altitudes was identified (p > .05). Samples taken from infected cattle were subjected to PCR analysis, which identified the genome of the virus most frequently in skin nodules (78%), nasal swabs (23.4%), blood (13%) and sera (14.5%). Interestingly, LSDV genome was occasionally identified in lung and milk samples. Based on the PRO30 sequence analysis, lumpy skin disease virus (LSDV) strains circulating in Russia were all identical and fell within the cluster of field LSDV found worldwide.