Interaction of iron oxide Fe3O4 nanoparticles and alveolar macrophages in vivo.

Aqueous suspension of magnetite nanoparticles with primary diameter of 10 nm were intratracheally administered into rat lungs. In 24 h, cells were isolated from bronchoalveolar lavage and examined under a transmission electron microscope. Alveolar macrophages demonstrated ability to actively uptake single nanoparticles and small aggregates composed of such particles, which then formed larger conglomerates inside fused phagosomes. Some of these mature phagosomes shed the membrane and free nanoparticles closely interacted with nuclear membrane and with cristae and mitochondrial membranes thereby inflicting pronounced damage to these intracellular structures. The loss of primary lysosomes can be viewed as indirect evidence attesting to the role played by diffusion of lysosomal hydrolytic enzymes in the final destruction of the alveolar macrophages provoked by nanoparticles.

[Comparative experimental assessment of the impact of gold and silver nanoparticles on the phagocyting cells of the lower airways].

Judging by the cytological characteristics of the free cell population of the lower airways obtained with assistance of the bronchoalveolar lavage in 24 hours after the intratracheal instillation of equal doses of equidimensional gold or silver nanoparticles, both metals result in active recruitment of phagocytes with domination of neutrophile leukocytes, especially marked after the instillation of the nanosilver. The higher ratio of these cells count to that of alveolar macrophages gives evidence for the significantly higher cytotoxicity of the nanosilver comparing with both nanogold and even the smallest silver particles in the micrometric range. Transmission electron microscopy demonstrates similar pictures of intracellular distribution and ultra-structural damages caused by internalized nanoparticles in both types of phagocytes, while there are significant differences between cells under impact of nanosilver vs. those under impact of nanogold. The highest importance is higher propensity of the nanosilver particles to aggregation and to ingression into mitochondria with damaging these organelles.

[Neuropathogenecity of Coxsackie B virus strains isolated from children with clinical manifestations of aseptic meningitis in different years].

The neuropathogenicity of Coxsackie B3, B1, and B5 virus strains was studied in experimentally infected suckling BALB/c mice and in contact animals from the same nest and litter infected due to the natural virus spread. The similar neurological disorders were found in both groups of animals. The data on pathological and morphological changes in the medulla oblongata as dystrophic and necrotic changes in the neurons with their lysis and deletion, brain tissue edema, and hemodynamic changes confirmed the neutrotropicity of the strains under study. The revealed pattern of brain lesions did not depend on the time of isolation of the viral strains being examined.

Experimental modeling of viral diseases of the locomotor system.

Dissemination of infectious inflammation was studied in experimental influenza and acute and chronic herpesvirus infections. The possibility of articular involvement into the infectious process was evaluated. Pathomorphological signs of changes in the articular tissue confirmed the effects of these viruses on the locomotor pathology. Results of virus infection simulation in experimental animals suggest this model for studies of the pathogenesis of diseases of viral etiology (including those with articular involvement) in humans.

[Central nervous system lesions in fetuses and newborns in intrauterine infection caused by respiratory viruses]. / Porazheniia tsentral'noi nervnoi sistemy plodov i novorozhdennykh pri vnutriutrobnoi infektsii, vyzvannoi respiratornymi virusami.

Congenital respiratory viral infection is followed in the CNS of fetuses and newborns by grave dyscirculatory disturbances with glia proliferation and nervous tissue edema. The process is mainly localized in the periventricular regions of the brain ventricles. Neurologic and morphologic consequences of these damages in the CNS of fetuses and newborns need further studies.

[Morphological diagnosis of intrauterine chlamydia infection and its clinico-anatomical characteristics]. / Morfologicheskaia diagnostika vnutriutrobnogo khlamidioza i ego kliniko-anatomicheskaia kharakteristika.

Clinicomorphological characteristics of intrauterine chlamydiasis (IUC) are given. The authors describe a cottonwool-like meningochorioiditis the observation of which at necropsy allows IUC suspection. Chlamydial etiology of this condition is confirmed by means of electron microscopy and immunofluorescence. Fibroblast proliferation of the pia mater followed by intensive fibrillogenesis plays a most important role in morphogenesis of cottonwool-like nodules. The occurrence of IUC at the necropsies varies depending on the age of foetuses and newborns from 6.2 to 38.7%.

[Ultrastructural pathology of the lymph nodes in tick-borne encephalitis]. / Ul'trastrukturnaia patologiia limfaticheskikh uzlov pri kleshchevom éntsefalite.

Lymph nodes of humans and experimental animals with tick-borne encephalitis (TBE) were studied using electron microscopy. TBE virus reproduction occurred in macrophages, reticular and plasma cells. Severe organelle destruction was found in the above cells and lymphocytes. The results suggest that macrophage, reticular and plasmatic cell death is due to the virus reproduction, while lymphocyte death is due to the toxic effect. It is evident that the outcome is determined by pathological process in lymphoid organs.

[Ultrastructural pathology of the placenta in respiratory-syncytial viral infection and mycoplasmosis]. / Ul'trastrukturnaia patologiia platsenty pri respiratorno-sintsitial'noi virusnoi infektsii i mikoplazmoze.

Electron microscopy of the placentas affected by respiratory-syncytial virus and mycoplasmas (Mycoplasma urealyticum) revealed the most pronounced alterations in the syncytiotrophoblast structures. Destructive changes in the respiratory-syncytial infection were associated with a direct reproduction of viral particles. Two types of alterations (acute and long-lasting) reflecting two stages of the infectious process are reported in the Mycoplasma infection.

[Ultrastructural pathology of congenital infection provoked by respiratory viruses]. / Ul'trastrukturnaia patologiia vrozhdennoi infektsii, vyzvannoi respiratornymi virusami.

The ultrastructural study of fetal and newborn lungs in the intrauterine infection caused by respiratory viruses showed the virus reproduction to take place in type II alveolocytes with destructive changes in cell organelles. Each type of virus results in a certain picture of ultrastructural changes. Progressing cell organelles destruction with an intensive cytoplasm vacuolization and virion presence in the cytoplasmic matrix and on the endoplasmic network membranes is characteristic for influenza. Severe cytoplasm vacuolization with lipid formation, homogenization and condensation of membranous bodies, nuclear pyknosis are observed in parainfluenza. RS-infection is characterized by virion formation on the cytoplasmic cell membrane, numerous deformed membranous bodies, filling intercellular spaces and alveolar lumen with rough granular electron-dense material, massive release of organelles into the alveolar lumen. Edema and vacuolization of endothelium, edema and focal disappearance of basal membrane are observed in the capillary walls.

[Ultrastructural pathology of the liver in abdominal typhoid]. / Ul'trastrukturnaia patologiia pecheni pri briushnom tife.

Light and electron microscopies were applied to examine liver punctates from 10 patients with typhoid fever. Both in the full swing of the disease and in clinical recovery (convalescence), dystrophic and necrobiotic changes along with focal cell death were found to occur in the hepatocytes, endothelial and Kupffer cells covering the sinuses. The protein-synthesizing system and mitochondria were demonstrated to be primarily destroyed. The microbes of typhoid fever were located in the hepatocytes, endothelial and Kupffer cells.

[Pathomorphology of uveitis caused by an echovirus]. / Patomorfologiia uveita, vyzvannogo virusom ECHO.

The monkey eyes infested by inoculation into the eye anterior chamber of the ECHO-19 virus from children with uveitis were studied morphologically. It was established electron microscopically that the inoculated virus is replicated in the capillary endothelium and stromal cells of the uveal tract. Crystal-like accumulation of virions and degenerative changes in the organelles are observed in these cells. Acute granulomatous alterative-exudative-hemorrhagic uveitis with the destruction of the iris, ciliary body and processes and secondary changes in the cornea and crystalline lens with the symptoms of keratitis and cataract develop in the anterior part of the eye as observed in the light microscope. The anterior and posterior goniosynechia develop. An acute inflammatory process is further transformed into a progressing autoimmune inflammation.

[Ultrastructural changes in the CNS of monkeys with the chronic form of tick-borne encephalitis]. / Ul'trastrukturnye izmeneniia v TsNS obez'ian pri khronicheskoi forme kleshchevogo éntsefalita.

The central nervous system of monkeys with chronic tick-borne encephalitis (TBE) shows the following ultrastructural alterations which differ from those in acute TBE: widespread destructive changes in neurons, astrocytes, oligodendrocytes, processes, myelin, vascular walls, severe edema of brain tissue with the signs of a so-called spongious degeneration and the absence of cell proliferation and perivascular cell infiltrations, glial nodules as well as circulatory disorders (hyperemia, stasis, hemorrhages). Few virions with or without and altered supercapsid membrane are detected in the neuronal cytoplasm or in the intercellular spaces; the signs of active virus reproduction in the cells are lacking. Pathologic process is of a degenerative but not of an inflammatory nature; the latter is typical for acute TBE.

[Ultrastructural changes in the central nervous system of mice in tick-borne encephalitis]. / Ul'trastrukturnye izmeneniia v tsentral'noi nervnoi sisteme myshei pri kleshchevom entsefalite.

Tick-borne encephalitis virus is localized in nerve cells and intracellular spaces. According to the nature of ultrastructural changes, the pathological process in nerve cells may be divided into three stages connected with the stages of virus reproduction. In the first stage, the protein-synthesizing systems of the cell are degraded. In the second stage specific virus inclusions form in the cell cytoplasm as aggregates of mature and immature virions alongside with destruction of ultrastructures and growth of smooth membranes. In the third stage degradation of neurons is accompanied by necrobiosis and discomplexation of the surrounding glial elements, processes, cells of the inflammatory infiltrate and capillary walls. A certain combination of nonspecific changes in organelles of various cells with viral inclusions makes the ultrastructural picture of the focus of lesions in tick-borne encephalitis sufficiently characteristic for differential pathological diagnosis.

[Ultrastructural changes in the central nervous system of monkeys in poliomyelitis]. / Ul'trastrukturnye izmeneniia v tsentral'noi nervnoi sisteme obez'ian pri poliomielite

The ultrastructure of cells of the central nervous system of Rhesus monkeys in experimental poliomyelitis caused by virus of poliomyelitis Type 3 was studied. It was found out that the virus of poliomyelitis was localized in nerve cells, astocytes, oligodendrocytes, the endothelium of capillaries and macrophages. This justifies the conclusion that pathological changes in the cells referred to the above result from reproduction of the virus therein. Ultrastructural changes in infected cells are divided into three stages: the first stage corresponded to eclipse-phase of infection; the second -- to the period of reproduction of the virus and composition of viral particles; and the third -- to the period following the escape of the virus from the cell. A definite combination of nonspecific changes in organoids of various cells with specific viral inclusions makes the ultrastructural picture of cells in poliomyelitis sufficiently characteristic for differential diagnosis. Pathogenesis of the developing lesions is discussed.