Search

The main reason for the weakening of the body of rabbits is a deficiency of nutrients and biologically ac􀆟ve substances in their diet. The search for non-toxic and highly effec􀆟ve preven􀆟ve drugs of complex ac􀆟on that have a posi􀆟ve effect on the metabolism of minerals in rabbits is of keen interest. Here we present the results of the study of morphological and biochemical parameters of the blood as well as the content of chemical elements in blood plasma in New Zealand White rabbits on the farm in Kyiv region. The paper presents the materials for determining the biochemical status of the body in fa􀆩ening rabbits for the preven􀆟on of microelementoses using a new experimental environmentally friendly tool. The content of total protein, albumin, glucose, total calcium, inorganic phosphorus, total bilirubin, urea, crea􀆟nine, TBA-ac􀆟ve products, Fe, Mn, Cu, Zn, Co and the ac􀆟vity of ALT, AST, LF, and HGT in the blood of New Zealand White rabbits in the first and 50th days of the experiment (before and a􀅌er the use of biologically ac􀆟ve addi􀆟ve "Huminorm plus") are presented here for the first 􀆟me. The use of this addi􀆟ve had a posi􀆟ve effect on haematopoiesis, protein and mineral metabolism, and func􀆟onal status of the liver, which indicates its high efficiency for the preven􀆟on of micronutrient deficiency. "Huminorm Plus" s􀆟mulates poten􀆟al body growth in rabbits up to the age of 90 days. [ABSTRACT FROM AUTHOR]

Silicone is used widely for tissue augmentation in humans. However, late complications, such as delayed inflammation and capsular contracture, remain uncharacterized, despite their importance. In the present study, we aimed to determine whether mechanical and thermal damage induce capsular inflammation around a foreign body, and elucidate the biological mechanism underlying this phenomenon. We injected silicone into the subcutaneous layer of the skin of New Zealand white rabbits. The rabbits were divided into two groups: the control group received no treatment; in the experimental group, external force was applied near the injection silicone using high-intensity focused ultrasound (HIFU). Tissues near the injected silicone were harvested from both groups on Days 4, 7, and 30 after HIFU treatment for comparative analysis. Visual and histological examinations showed clearly increased inflammation in the experimental group compared with that in the control group. Furthermore, capsular tissue from the experimental group displayed markedly increased collagen production. Immunofluorescence revealed marked activation of macrophages in the early stages of inflammation (Days 4 and 7 after HIFU treatment), which decreased on Day 30. Assessment of cytokine activation showed significantly increased expression of heat shock protein (HSP)27, HSP60, HSP70, toll-like receptor (TLR)2, TLR4, and interleukin-8 in the experimental group. The expression of transforming growth factor-β1 did not increase significantly in the experimental group. In conclusion, damage to tissues around the injected silicone induced capsular inflammation. Macrophages and damage-associated molecular pattern molecules were involved in the early stages of inflammation. HSP release activated TLRs, which subsequently activated innate immunity and induced the inflammatory response. [ABSTRACT FROM AUTHOR]

B-cell chronic lymphocytic leukemia (CLL) remains an incurable disease, and despite the improvement achieved by therapeutic regimes developed over the last years still a subset of patients face a rather poor prognosis and will eventually relapse and become refractory to therapy. The natural rotenoid deguelin has been shown to induce apoptosis in several cancer cells and cell lines, including primary human CLL cells, and to act as a chemopreventive agent in animal models of induced carcinogenesis. In this work, we show that deguelin induces apoptosis in vitro in primary human CLL cells and in CLL-like cells from the New Zealand Black (NZB) mouse strain. In both of them, deguelin dowregulates AKT, NFκB and several downstream antiapoptotic proteins (XIAP, cIAP, BCL2, BCL-XL and survivin), activating the mitochondrial pathway of apoptosis. Moreover, deguelin inhibits stromal cell-mediated c-Myc upregulation and resistance to fludarabine, increasing fludarabine induced DNA damage. We further show that deguelin has activity in vivo against NZB CLL-like cells in an experimental model of CLL in young NZB mice transplanted with spleen cells from aged NZB mice with lymphoproliferation. Moreover, the combination of deguelin and fludarabine in this model prolonged the survival of transplanted mice at doses of both compounds that were ineffective when administered individually. These results suggest deguelin could have potential for the treatment of human CLL. [ABSTRACT FROM AUTHOR]