Serum Concentrations of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor, Nitric Oxide and Endothelial DNA Proliferation in Development of Microvascular Pathology in Acute African Swine Fever.

There is significant evidence that pathology of the microcirculation occurs in African swine fever (ASF); however, the mechanisms by which it develops are largely unknown. In the present experimental infection study, we show that an increase in vascular permeability in the initial stages of acute ASF is dependent on viraemia and elevation of the concentration of serum nitric oxide (NO). Macrophages activated by ASF virus (ASFV) are stimulated to produce NO and simultaneously to sensitize the endothelial cells through the action of vascular endothelial growth factor Β (VEGFΒ), which is followed by an increase in VEGF-mediated endothelial permeability. In the later stages of disease, the endothelial cells undergo DNA proliferation, which may additionally provoke capillary leakage, point haemorrhages and migration of blood cells into tissues. The possible mechanism of a shift in the cell cycle from the G1 to S and G2 stages could be a direct effect of ASFV. The terminal stages of disease are characterized by triggering of compensatory mechanisms such as stimulation of the synthesis of stromal cell-derived factor-1.

[Effect of human brain extracts on cultured neuroblastoma cells]. / Vliianie ékstraktov golovnogo mozga cheloveka na kletki kul'tury neiroblastomy.

OBJECTIVE: To identify the effect of brain extracts from people of different age groups on possible changes in cell physiology and behavior in vitro. MATERIAL AND METHODS: Human frontal cortical segments were obtained 12-24 hours after autopsy. Brain tissue extract was taken from young people who died at age of 22.5±2.7 years and old people at 80.9±3.0 years. SK-N-MC human neuroblastoma cells were cultured in a medium containing 50 mg/ml of brain tissue extracts; blood serum (50 mg/ml) from healthy people was used as a control. Procedures for cytophotometry of DNA and acidic proteins and polarized light microscopy were used. RESULTS: A short-term decrease in acidic protein levels in the nucleus and nucleolus was found to be affected by brain extracts from old people. There were higher cytoplasmic acidic protein levels. At the same time, the same indicators generally remained noticeably unchanged under the influence of brain extracts from young people. There were also simultaneous pronounced changes in cell morphology and behavior in vitro; namely, neuronal cell processes became shorter and their proliferative activity increased, which was not least a result of the unblocking of cells in the G2 phase under the influence of brain extracts from old people. CONCLUSION: The factors that accelerate cell proliferation in vitro accumulate in the human brain with age. Simultaneously with the acceleration of cell proliferation, there are changes in cell metabolic activity and morphology.

Hemophagocytic lymphohistiocytosis in acute African swine fever clinic.

INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) usually has been defined as the combination of a proliferation of cytologically benign, actively phagocytic macrophages in bone marrow, spleen, lymph nodes, etc. in association with fever, cytopenia, splenomegaly, and hypertriglyceridemia. HLH is often triggered by viral infection. The aim of this study was to ascertain the features of HLH involvement in African swine fever virus (ASFV) (genotype II) pathogenesis. METHODS: The serum levels of macrophage colony-stimulating factor (MCSF) and granulocyte-macrophage colony-stimulating factor (GMCSF), as well as the histological constitution (for hemophagocytic macrophages detection) of various organs of pigs infected with ASFV genotype II were investigated. The diagnosis of HLH was made according to universally accepted human criteria. RESULTS: The association of fever, cytopenias, splenomegaly, and hemophagocytosis was present in 87.5% of the infected pigs (absence of hyperthermia in one of eight pigs). Marked hypertriglyceridemia was observed at 3-4days post infection. Previously it was shown that ASFV induced a significant decrease in the level of fibrinogen from day 5 till the end of experiment. Progression of the HLH coincided with a temporary increase in the serum levels of MCSF levels (early stage of disease) and GMCSF levels (2-3 pays post infection). CONCLUSIONS: Hemophagocytic syndrome should be suspected in ASFV (genotypeII) infected pigs.