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.

Reconstruction of rabbit urethral epithelium with skin keratinocytes.

We have investigated the living skin equivalent (LSE) as an alternative source of plastic material for closing full-thickness epithelial-stromal urethral injuries. The possibility of transdifferentiation of epidermal keratinocytes, a component of 3D tissue constructs, was investigated in vivo in a model of the recovery of urethral injuries in laboratory rabbits. Autologous grafting of LSE in de-epithelialized urethra showed that skin keratinocytes placed in a specific in vivo microenvironment can be incorporated into the damaged area and function as urothelium. The use of EGFP transfected keratinocytes allowed us to identify transplanted cells. The reconstructed urethral tubes did not develop strictures or fistulas at the site of the grafted LSE. Immunohistochemical studies of neo-urothelium revealed EGFP-positive cells expressing the urothelial markers K7 and UP3.

Culicoides biting midges (Diptera, Ceratopogonidae) in various climatic zones of Russia and adjacent lands.

Culicoides biting midges play an important role in the epidemiology of many vector-borne infections, including bluetongue virus, an internationally important virus of ruminants. The territory of the Russian Federation includes regions with diverse climatic conditions and a wide range of habitats suitable for Culicoides. This review summarizes available data on Culicoides studied in the Russian Federation covering geographically different regions, as well as findings from adjacent countries. Previous literature on species composition, ranges of dominant species, breeding sites, and host preferences is reviewed and suggestions made for future studies to elucidate vector-virus relationships.

[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.

[Regulation of potential-dependant calcium channels by 5-HT1B serotonin receptors in various populations of hippocampal cells].

Metabotropic serotonin receptors of 5HT1-type in brain neurons participate in regulation of such human emotional states as aggression, fear and dependence on alcohol. Activated presynaptic 5-HT1B receptors suppress the Ca2+ influx through the potential-dependent calcium channels in certain neurons. The Ca2+ influx into the cells has been measured by increase of calcium ions concentration in cytoplasm in reply to the depolarization caused by 35mM KC1. Using system of image analysis in hippocampal cells culture we found out that Ca2+-signals to depolarization oin various populations of neurons differed in form, speed and amplitude. 5HT1B receptor agonists in 86 +/- 3 % of neurons slightly suppressed the activity of potential-dependent calcium channels. Two minor cell populations (5-8 % of cells each) were found out, that strongly differed in Ca2+ signal desensitization. Calcium signal caused by depolarization in one cells population differed in characteristic delay and high rate of decay. 5HT1B receptor agonists strongly inhibited the amplitude of the Ca2+ response on KCl only in this population of neurons. The calcium signal in second cell population differed by absence desensitization and smaller amplitude which constantly increased during depolarization. 5HT 1 B receptor agonists increased the calcium response amplitude to depolarization in this population of neurons. Thus we show various sensitivity of potential-dependent calcium channels of separate neurons to 5HTB1 receptor agonist.

[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.

[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.

[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.

[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).

[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.

[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.

[Clinical course of Helicobacter pylori associated chronic gastritis in post-eradicational period].

Results of a prospective cohort study of Helicobacter pylori associated chronic gastritis in posteradicational period have been analyzed in the paper. Different versions and prognostic markers in posteradicational period were identified. Curation algorithm for a patient with chronic gastritis after antihelicobacter therapy was suggested.

[Inflammation as a basis for Helicobacter pylori-associated diseases].

The molecular-cellular features of gastric mucosal inflammation caused by Helicobacter pylori are formulated. Chronic gastritis is considered as the morphological basis of gastric ulcer and non-cardial cancer of the stomach of intestinal type. The basic influences of the products of a pathogenicity island of bacterium (Cag A-protein) and VacA-cytotoxin on the gastric mucosa, as well as bacterial genetic polymorphism are discussed. The evolution of the phenotypes of chronic gastritis-- "ulcerative" "cancerous" is analyzed. Helicobacter pylori-associated inflammation may depend on the host's inflammatory response which in turn is determined by the allelic polymorphism of cytokine genes rather than the genetic characteristics of a bacterial strain.

[Morphology of surface and atrophic gastritis in eradication of Helicobacter pylori (HP)].

It is shown with the use of immunohistochemical detection of Bcl-2, caspase-3 and Ki-67 that eradication of HP does not result in immediate reverse development of atrophic changes. This depends on duration of persistence of mononuclear inflammatory cells.

[Interpretation of the notion "dysplasia/ intraepitelial neoplasia" in the international classification of tumors].

The review of international classification of tumors of digestive tract is presented: that of Padua (1998), Wien (1998, 2002), WHO (2000). Principal definitions are considered, the content of terms "dysplastic" and "neoplasia" is analysed. The attempt to systematize the description of morphological picture of neoplasia (adenoma/dysplasia) of low and high degree and difference of uncertain neoplastic (dysplasia) from true neoplastic changes. Principles of clinical interpretation of biopsies are presented.

[Clinical and pharmacoeconomic aspects of the antisecretory therapy of gastroesophageal refluxed disease]. / Klinicheskie i farmakologicheskie aspekty antisekretornoi terapii gastroézofageal'noi refliuksnoi bolezni.

The article discloses the results of an open prospective randomized study of the antisecretory therapy efficiency conducted among 20 patients with gastroesophageal refluxed disease (erosive form, non-complicated course). The selection of the optimal antisecretory drug was substantiated from the point of view of the clinic-diagnostic and pharmacoeconomic assessment of the results of the above-mentioned therapy conducted with the application of rabeprosole (pariet) and its generic omeprosole (omez).