Infectious bursal disease virus: identification of the novel genetic group and reassortant viruses

The results of the phylogenic analysis of the nucleotide sequence of the IBDV A and B genome segments have been presented. Traditionally the IBDV isolates are classified based on the phylogenic analysis of the hypervariable region of the VP2 gene. The analysis of the VP2 gene segments of the isolates detected in the Russian Federation demonstrated that most of them belong to the genetic group comprising highly virulent IBDV isolates. However, not all isolates belonging to one genetic group have the same phenotypic characteristics. This is related to the fact that the virulence is determined not only based on the characteristics of the VP2 gene (A segment) but on the characteristics of the VP1 gene (B segment) as well. The IBDV genome segmentation allows formation of reassortant viruses which can be identified as a result of the genome segment analysis. The phylogenic analysis of the nucleotide sequences of VP2 and VP1 genes of 28 IBDV isolates detected at RF, Ukrainian and Kazakh poultry establishments in 2007 and 2019 showed that 15 of them are reassortant viruses. Different combinations of the genome segments have been identified among these reassortant viruses. Detection of different combinations of IBDV genome segments is indicative of the fact that the heterogeneous virus population circulates on the poultry farms. Pathogenicity studies of the three IBDV isolates showed that the most virulent was an isolate having two genome segments characteristic of the highly virulent virus. Two reassortant viruses having only one genome segment A or B, characteristic of the infectious bursal disease, demonstrated less pronounced virulent properties

HYPERURICEMIA CORRECTION IN MEN WITH METABOLIC SYNDROME: ACARBOSE POTENTIAL

The study was aimed at the investigation of “test” (6 days) and longer-term (8 weeks) acarbose treatment effects on plasma uric acid (UA) concentration in patients with metabolic syndrome (MS). Material and methods. In total, 33 men with MS and carbohydrate metabolism disturbances were administered 6-day “test” acarbose therapy. At baseline and 7 days later, saccharose tolerance test was performed, with the measurement of venous plasma levels of fasting UA, fasting fructose, glucose (fasting, 60 and 120 minutes after saccharose load), and insulin (fasting and 120 minutes after the load). 4 weeks later, 20 patients were administered 8-week acarbose therapy, with standard gradual dose increase. At baseline and after the treatment, venous plasma concentrations of UA and fructose were measured. Results. Hyperfructosemia was observed in 100% of the patients, with mean plasma fructose concentration of 0,82±0,97 mmol/l. Hyperuricemia was observed in 51,5% (n=17), with mean plasma UA concentration of 413,2±86,5 mmol/l. Six-week acarbose therapy resulted in a significant decrease of UA levels (p=0,0015) and fructose levels (p=0,049), as well as in postprandial levels of glucose (p=0,03) and insulin (p=0,013). Eight-week acarbose therapy was associated with mean decrease of plasma UA concentration by 5,8% (p=0,04), but no significant changes in fasting plasma levels of fructose (p>0,05)

Impact of 5-Azacytidine on placental weight, glycoprotein pattern and proliferating cell nuclear antigen expression in rat placenta

During the placentation process, the expression of various glycoproteins plays an important role in embryonal development. Alterations in DNA methylation caused by 5-azacytidine (5azaC) can disturb normal glycoprotein expression as well as the proliferative ability of trophoblast cells. In order to assess this, a single dose of 5azaC was injected intraperitoneally into pregnant rats during days 1-19 of gestation. Animals were euthanised on day 20 and placental weight, as well as glycoprotein composition, was analysed together with immunohistological assessment of the degree of proliferation of the trophoblast cells. The placental weight was found to be significantly smaller in animals treated by 5azaC during days 4 to 14 of gestation (p<0.01, Student's t-test). The treatment on days 4, 5, and 6 resulted in a lack of labyrinth with the strong proliferative activity of the cells in the basal layer. Expression of glycoproteins with molecular mass smaller than 60kDa was reduced with treatment on day 6. The 5azaC administered from days 7 to 10 completely disturbed the placental structure and the proliferation of trophoblast cells was poor. During these days GP70 exhibited stronger expression in treated animals, contrary to GP40, which was stronger in controls. A natural border between the labyrinth and the basal layer was established on days 11 and 12. The basal layer was dominant with a lower proliferation of trophoblast cells compared with the controls. With the establishment of the labyrinth on day 13, the expression of GP40 was restored. Proliferation of the trophoblast cells from days 13 to 15 was higher compared with the controls. The changes in placental mass and the proliferative ability of trophoblast cells in rat placenta exposed to 5azaC represent more proof of the importance of epigenetics in the regulation of placental development

Galectin-3 and matrix metalloproteinases 2 and 9 in peripheral blood of gastric cancer patients

Background: High incidence of gastric cancer (GC), its aggressive clinical course, rapid tumor dissemination, low sensitivity to chemotherapy and lack of reliable laboratory diagnostic criteria urgently require a search for the most informative markers associated with key biologic properties of the tumors. Aim: Comparative analysis of galectin-3, matrix metalloproteinase (MMP)-2, and MMP-9 levels in peripheral blood of GC patients and healthy donors, assessment of association of these markers with clinical morphological characteristics of the disease, and prognosis of overall and relapse-free survival. Materials and methods: Sixty (60) primary treatment-nave GC patients (38 men, 22 women) aged 29 to 81 years and 90 healthy donors compatible with their age and sex were included into the study. Galectin-3 was measured in EDTA plasma, MMP-2 and MMP-9 in serum with standard direct enzyme immunoassay kits "Human MMP-2 (total)", "Human MMP-9 (total)", "Human Galectin-3" (RD Systems, USA). Results: Plasma galectin-3 concentration in the GC patients was significantly higher than in the healthy controls (median 12.9 and 10.6 ng/ml, respectively; p 0.0001). No difference in serum MMP-9 levels between GC patients and control subjects were found, while MMP-2 level in the control group was significantly higher, than in the GC patients (p = 0.039). No association between galectin-3, MMP-2, and MMP-9 blood levels in the GC patients could be identified. In contrast to GC patients, there was a positive correlation of plasma galectin-3 with age in the control group (rs = 0.51, p 0.005). No associations between the biomarkers levels in blood and clinical and morphological characteristics of GC were established, except MMP-9 being higher at Т4а invasion depth as compared to the earlier Т2 level. Marked differences in the overall survival depending on plasma galectin-3 levels were found, with the cut-off level of 12.9 ng/ml: the 5-year overall survival in the patients with low galectin-3 was better, than in those with its higher level (50 and 43%, respectively; however, the difference was non-significant, р 0.1). Both overall and relapse-free survival of the GC patients was higher in those with low ( 212 ng/ml) serum MMP-2: the 5-year overall survival in this group comprised 60% versus 23% in the patients with higher MMP-2 (p = 0.018). The difference in relapse-free survival was non-significant. Serum MMP-9 levels had no significant impact on the survival of GC patients. Conclusion: The ambiguous data on the clinical role of galectin-3, MMP-2, MMP-9 in GC obtained in this study indicate the necessity of further investigation of their possible utility for the diagnostics and prognosis of treatment results

Ultrastructural changes in the interhaemal membrane and junctional zone of the murine chorioallantoic placenta across gestation

The mouse is an extremely useful experimental model for the study of human disease owing to the ease of genetic and physiological manipulation. A more detailed knowledge of murine placental development will, we hope, increase our understanding of the pathogenesis of placentally related complications of human pregnancy. The murine placenta consists of two main fetally derived compartments: the labyrinthine zone and the junctional zone. Exchange in the labyrinthine zone takes place across an interhaemal membrane comprising an outer layer of cytotrophoblast cells and two inner layers of syncytial trophoblast. The cytotrophoblast layer thins as gestation advances, and in addition becomes highly perforated after embryonic day (E)12.5. Furthermore, as gestation advances cytotrophoblast nuclear volume and DNA content increase, suggesting the formation of labyrinthine trophoblast giant cells. The syncytial layers become increasingly microvillous, enlarging the surface area for exchange. Separate basement membranes support the syncytium and the fetal capillary endothelium throughout gestation, although these appear to fuse where the capillaries are closely approximated to the trophoblast. The junctional zone consists of two principal trophoblast cell types, spongiotrophoblasts and invasive glycogen cells, yet the functions of each remain elusive. Spongiotrophoblasts vary in their appearance even when not fully differentiated, but a striking feature is the extensive endoplasmic reticulum of the more mature cells. Early glycogen cells are distinguished by the presence of electron-dense glycogen granules, and large amounts of surrounding extracellular matrix. Later the accumulations of glycogen granules occupy almost all the cytoplasm and there are few organelles. This is the first study to use both scanning and transmission electron microscopy in an ultrastructural description of murine placental development and is complementary to contemporary genetic investigations