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Experimental model in ovo. Glioblastoma multiforme (GBM) is the most common primary malignancy in the brain and confers a uniformly poor prognosis. Despite decades of research on the topic, limited progress has been made to improve the poor survival associated with this disease, new therapeutic strategies are still needed. The application of nanotechnology to disease treatment, diagnosis, monitoring, drug delivery platform and to the control of biological systems is promising, also in cancer therapy. Diamond na-noparticles (DN) are bioactive substance toward glioma tumour cultured on the chicken embryo chorioallantoic membrane (CAM). DN reduce tumor mass and volume and inhibited new blood vessel development in glioma tumor. In the present experiment we additionally observed, that DN caused changes in the tumor ultrastructure testify to the ongoing process of cell death, probably carried out by autophagy.
The aim of this study was to compare the most commonly-used experimental models and to assess the microscopic renal changes in different models of cyclosporine A (CsA) nephrotoxicity. Wistar male rats were divided into five groups, eight animals in each. CsA was given in doses of 15 mg/kg, 25 mg/kg, and 100 mg/kg, respectively. The blood was collected for creatinine, urea, and uric acid levels analysis in the serum and the kidneys were sampled for microscopic examination on the 11th and 29th d of the experiment. CsA induced nephrotoxicity was characterised by increased serum levels of creatinine, urea, and uric acid. Microscopic features of CsA nephrotoxicity in all CsA experimental groups were observed. We would recommend the use of low doses of CsA for approximately 28 d as the most relevant experimental procedure for achieving the features of chronic CsA nephrotoxicity.
Background. The aim of this study was to investigate the possibility of using sodium selenite as a treatment for acute glyphosate poisoning using the activity of the lipid peroxidation and antioxidant defence systems as a readout for efficacy. Material and methods. Experimental glyphosate poisoning and subsequent treatment using sodium selenite was performed in albino rats (105). Glyphosate was given in doses of 50, 100 and 130 mg/kg, and sodium selenite was administered at a dose of 2 μg/kg. The blood concentrations of lipid peroxidation markers including conjugates of diene andtrienoic and malondialdehyde were determined. The endogenous glutathione (reduced form) level and activities of catalase, superoxide dismutase and glutathione peroxidase in the serum were measured. Results. Glyphosate poisoning has been found to result in a significant increase in lipid peroxidation activity. For example, malonic dialdehyde demonstrates a 2.35 times increase at a glyphosate dose of 130 mg/kg. At the experimental glyphosate poisoning dose of 100 mg/kg the measurements of superoxide dismutase and glutathione peroxidase have been found to decrease 1.58 and 2.21 times, respectively. At a dose of 130 mg/kg, those values decreased 2.51 and 4.76 times, respectively, compared to untreated controls. Conclusions. The use of sodium selenite at a dose of 2 μg/kg after poisoning of white rats with glyphosate (at doses of 50, 100 and 130 mg/kg) normalizes the lipid peroxidation and antioxidant defence activities of the body.
Bioactive sphingolipids are important molecules that control wide spectrum of neuronal processes including neurotransmission, synaptic function, cells proliferation and death. Sphingosine kinases (SK1/2) are conserved enzymes that phosphorylate sphingosine to sphingosine-1-phosphate (S1P), which acts as a primary and secondary messenger. S1P binds to 5 receptors and plays essential role in neural signal transduction under physiological and various pathological conditions. Although growing evidence suggests important role of SK1/2 and S1P in neurodegenerative disorders including ischemia, inflammation and Alzheimer’s Disease, till now disturbances of sphingolipids homeostasis in Parkinson’s Disease (PD) remain unknown. Our study try to explain the role of SK1/2 and S1P in molecular mechanism of cell survival and death in model of oxidative stress evoked by neurotoxin 1-methyl-4-phenylpyridinium (MPP+), compound widely used in experimental model of PD. Our data presented that MPP+, comparable to SK inhibition evoked death of human neuroblastoma cells SH-SY5Y in time and concentration dependent manner. These changes are accompanied by increased free radicals concentration in these cells. Reduced level of SK1 protein was detected in SH-SY5Y cells after 24h exposure to MPP+ comparing to control. Moreover S1P pretreatment enhanced survival of these cells and protein level of SK1 comparing to MPP+ treated cells. Our data indicated that MPP+ evoked neuronal death is mediated by SK1/2 inhibition and altered sphingolipids signaling. These molecular events lead to caspase dependent apoptotic cells death and poly(ADP-ribose) polymerase-1 (PARP-1) degradation. All above results presented the alteration of sphingolipid biostat in experimental model of PD and suggested that S1P can offer novel, protective strategy.Supported by NCN Grant 5870/B/PO1/2011/40
The adaptation and immunogenisity of Cryptosporidium parvum isolated from Siberian chipmunks (SC1 strain) in immunocompetent (ICR) mice were examined. The oocysts were received to the severe combined immunodeficiency (SCID) mice by repeated passage. The oocysts collected from the 18th SCID mice were inoculated to 5 ICR mice. The mice began to shed oocysts from 6 days after inoculation, the patency was 5 days, and the maximum oocysts per gram of feces (OPG) value was 104. The maximum of OPG value was gradually increased by successive passage, and finally that in the 22nd mice reached 106 (patency: 11 days). It is considered that these results indicate completion of their adaptation to ICR mice. To examine the immunogenicity of C. parvum to ICR mice, 8 groups of 5 mice each were inoculated with 1.3 × 106 oocysts of SC1 strain, which were collected after adaptation to SCID mice. All groups shed oocysts from 6th day, and their patency was from 8 to 12 days. On the 21st day after the primary infection, these mice were challenged with 1.3 × 106 oocysts. No oocysts shed from any groups, although 2 control groups shed oocysts from the 6th day, and their OPG values were more than 106. These results suggest that this strain has strong immunogenicity against ICR mice. Therefore, the immunological healthy mice were considered a useful experimental model to investigate immunological and drug treatments in the strain of C. parvum.
Echinostomatidae (Trematoda) is the largest family within the class Trematoda. Members of this family have been studied for many years in relation to their utility as basic research models in biodiversity and systematics and also as experimental models in parasitology since they offer many advantages. Echinostomes have contributed significantly to numerous developments in many areas studied by parasitologists and experimental biologists. In this review, we examine the history of the echinostomebased studies from the beginnings to the present. For this purpose, we have divided the history of echinostomes into four periods (i.e. 18th and 19th centuries, first half of the 20th century, second half of the 20th century and the late 20th and 21th century) according to the types of studies performed in each of them. Moreover, we also briefly review the history of echinostome infections in humans.
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