OBJECTIVE: The objective of the study was to determine the specifics of the stromal and parenchymal liver components of 0–6-month-old children from HIV-monoinfected mothers. METHODS: The morphometric investigation included 84 liver tissue biopsies of 0–6-month-old dead children from HIV-monoinfected mothers. All morphometric parameters of the parenchymal and stromal liver components were calculated using the Avtandilov’s microscopic morphometric grid, which was consisted of 100 equidistant points. It was inserted into the microscope’s ocular tube with a total ×200 microscope magnification. The number of points that were found on the corresponding types of parenchymal and stromal liver components was calculated. In every case, it was selected 10 random microscopic areas and then all data were obtained, calculated, and presented as percentages. RESULTS: Morphometric parameters of hepatocytes: Mononuclear hepatocytes – 87.3 ± 6.2% (control – 93.5 ± 7.1), two-nuclear hepatocytes – 12.7 ± 1.3% (control – 6.5 ± 1.2), two-/mononuclear hepatocytes coefficient – 0.14 ± 0.01 (control – 0.06 ± 0.01), and hepatocytes with fat vacuoles – 15.6 ± 1.8% (control – 0.5 ± 0.2). Parenchymal and stromal liver components: Parenchyma – 64.3 ± 2.1% (control – 74.2 ± 1.3), stroma (including blood vessels and bile ducts) – 35.7 ± 1.9% (control – 25.8 ± 1.6), and stroma/parenchyma index – 0.55 ± 0.01 (control – 0.34 ± 0.01). Morphometric parameters of all of the liver components: Hepatocytes – 64.3 ± 3.1% (control – 74.2 ± 4.3), portal tracts – 14.9 ± 1.9% (control – 3.1 ± 0.6), central veins – 9.3 ± 1.3 % (control – 9.3 ± 1.4), sinusoids – 8.8 ± 1.1% (control – 10.5 ± 1.3), and bile ducts – 2.7 ± 0.2% (control – 2.9 ± 0.2). Expression level parameters: Fibronectin – 64.8 ± 4.1% (control – 17.3 ± 2.5), collagen Type I – 13.6 ± 1.7% (control – 9.7 ± 1.9), collagen Type III – 15.3 ± 1.4% (control – 10.1 ± 0.9), and collagen Type IV – 6.8 ± 0.2% (control – 5.9 ± 0.2). CONCLUSIONS: It was established that in the liver of 0–6-month-old dead children from HIV-monoinfected mothers, the parenchymal component of the liver showed the signs of its reduction, increase of regenerative activity of hepatocytes, and fatty degeneration of hepatocytes with a certain sign of reactive steatohepatitis. Furthermore, it was established that the stromal component of the liver of children from HIV-infected mothers showed the signs of its progressive proliferation and collagenization due to increased production and accumulation of fibronectin, Type I, Type III collagens in the stroma of portal tracts and newly formed septa, and the signs of hepatic sinusoid capillarization due to Type IV collagen accumulation in the space of Disse of the hepatic sinusoids.
The purpose of the study was to identify pathomorphic features of rat liver at different stages of postnatal ontogenesis caused by acute postnatal hypoxia. Materials and methods. All animals were divided into two groups C (control) and APH (acute postnatal hypoxia). Group C included 33 WAG line rats born from females with physiological pregnancies whereas group APH included 37 WAG line rats. Healthy rats of group APH were exposed to "alpine hypoxia" immediately after birth. The rats in both research groups were withdrawn from the experiment on days 1, 14, and 35 after their birth. The research material was the liver of experimental animals of both groups obtained at autopsy. Results and discussion. Having analyzed the morphometric parameters of group C hepatocytes, it can be stated that in the process of formation and maturation of liver beams there is an increase in the size of hepatocytes, which indicates the morphological and functional maturation of the tissue. According to the value of NCI (nuclear cytoplasmic index) in group APH1 there was an increase in the diameter of hepatocytes due to an increase in cytoplasmic volume, which can be explained by the instantaneous response of hepatocytes to acute hypoxia, manifested by metabolic imbalance and cell swelling. It should be noted that after the cessation of acute hypoxia, the size of hepatocytes gradually normalizes (groups AHP2-3). A significant (p <0.05) decrease in the total number of hepatocytes due to their mononuclear forms was also observed in the liver of APH1-3 group rats. In group APH3, on the 35th day after birth, the restoration of the structural and functional integrity of the liver occurred due to an increase in the number of binuclear hepatocytes, and was manifested by nearly two-time-increase in their number. Conclusion. The simulated acute postnatal hypoxia of rat descendants from healthy mothers caused a failure of compensatory capabilities with a sharp suppression of morphofunctional activity of the liver on day 1 of the experiment. The diameter of hepatocytes of the descendants exposed to acute postnatal hypoxia was significantly larger on day 1 (25.52±2.5 μm), and gradually normalized on days 14 (27.11±2.8) and 35 (38.94±3, 1 μm) after birth. The number of hepatocytes in the field of view in rats of acute postnatal hypoxia group progressively decreased on days 1 (198.7±13.1 cells), 14 (170.2±11.8 cells) and 35 (152.5±13.8 cells) after birth. The ratio of the number of binuclear hepatocytes to the number of mononuclear hepatocytes in rats of acute postnatal hypoxia group progressively increased on days 1 (0.02±0.01), 14 (0.05±0.01) and 35 (0.10±0.01) after birth
The aim: To identify immunohistochemical and morphometric features of chorionic trophoblast cells and fetal membranes derived decidual cells, which were obtained from stillbirths associated with pre-eclampsia, iron deficiency anemia, and acute chorioamnionitis. Materials and methods: The study included 58 fetal membranes of fetuses, who died in the ante-intranatal period. The membranes were divided into 6 obstetric history-based groups: premature (n = 8) and full-term (n = 8) stillbirths complicated by preeclampsia; premature (n = 8) and full-term ( n = 8) stillbirths complicated by iron deficiency anemia, premature (n = 10) and full-term (n = 16) stillbirths complicated by chorioamnionitis. A control group consisted of 8 membranes obtained from physiological pregnancies followed by the birth of a live full-term baby. Samples (rupture site) were probed with cytokeratin to identify the fetal trophoblast layer of the chorion and with vimentin for further identification of the decidual cells. The thickness of the trophoblastic layer, expression levels of cytokeratin and vimentin were determined. Results: A decrease of the cytokeratin expression by the chorionic trophoblasts and a thinning of the chorionic trophoblast cell layer due to an increasing gestational age were shown in case of the mentioned pathological conditions. In comparison with the control group, the level of vimentin expression by decidual cells was increased in case of full-term pregnancy complicated by preeclampsia, decreased in pregnancies complicated by chorioamnionitis, and remained unchanged in case of accompanying anemia. Conclusions: The changes in the studied immunohistochemical parameters are more pronounced in case of chorioamnionitis, which indicates more severe morphological and functional changes.
The aim: Determination of anatomical and topographical relationships of the eyeball anterior segment structures to assess possible glaucoma development risk factors in SED patients with myopic refraction. Materials and methods: Patients, aged from 10 to 34, have been examined since 2009. All the patients have undergone required medic and genetic examination as well as generally accepted ophthalmological one. Ultrasound biomicroscopy (UBM) has been performed using the VuMax II apparatus (Sonomed, USA) with a sensor frequency of 50 MHz. Results: Biomicroscopy found no symptoms such as pigment dispersion on the iris stroma, in the chamber anterior angle, iris transillumination and “Krukenberg’s Spindle”, which are characteristic for the ultrasound picture in pigment dispersion syndrome. Conclusions: 1. Clinical and functional study with the eyeballs mandatory ultrasound biomicroscopy have revealed functional space limitations for the structures of the iridociliary zone in patients with myopic type of eye structure in SED. 2. Detected congenital changes in the anterior segment structures (iridociliary cystic formations and residual mesodermal tissue) can lead to the emergence of intraocular blocks. 3. The research has identified conducive anatomical and topographic changes, which are likely to induce pigment dispersion syndrome or lead to the development of pigmentary glaucoma. 4. In our opinion, the UBM role in the early diagnosing and monitoring patients with SED syndrome is quite significant in terms of assessing the stability or dynamics of the changes received and possible complications. Ultrasound biomicroscopic scanning should be added to the list of necessary early diagnostic examinations to determine the markers and features of structures in SED.
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