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We studied the effect of the anticancer drug Ukrain on Lewis carcinoma in C57BL/6 mice. A marked progressive anticancer and antimetastatic effect was observed. On day 33 of tumor development, the tumor growth inhibition and metastases inhibition index were 71.5% and 73.1%, respectively. The antimetastatic effect of the drug manifested as a decrease in both number and volume of lung metastases. This finding demonstrates that treatment with Ukrain in Lewis carcinoma-bearing mice not only prevents the formation of new metastases but also inhibits the growth of existing ones. In addition to possessing anticancer and antimetastatic effects, Ukrain has been demonstrated to affect parameters characterizing the state of the immune system. This effect manifested as an increase in the endocrine function of the thymus (a central organ of the immune system), an increase in serum interferon, adhesion of peritoneal macrophages and formation of antibodies against thymus-dependent antigen by spleen plasma cells. Together with intensification of functional activity of the immune system, Ukrain increased the number of lymphoid cells and monocytes in peripheral blood. In addition to the increase in lymphocytes, the number of large granular lymphocytes also increased, i.e., cells possessing natural cytotoxic activity. The results obtained suggest that the antitumor, and especially the antimetastatic, effect of Ukrain is due to its immune-modulating properties, specifically, activation of antitumor resistance concerned with release of interferon and thymus humoral factors. Natural killer (NK) activity is one part of this resistance. NK cells are able to recognize and eliminate from the circulation cells with the potential to form metastases.  相似文献   
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Disorders in the immune system manifesting in decreased weight and cellularity of lymphoid organs, decreased count of large granular lymphocytes, suppression of the immune response and metabolic activity of macrophages were observed in experimental animals 1-6 months after thyroidectomy. The intensity of these disorders depends on the period elapsed after the surgery. These disorders can result from not only changes in the levels of the pituitary-thyroid hormones, but also disturbances in the endocrine function of the thymus in thyroidectomized animals.  相似文献   
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BACKGROUND: Exposure to Aspergillus fumigatus allergens results in enhanced total serum IgE and peripheral blood eosinophils in mice. The associated pulmonary inflammation and immunologic responses are comparable to those detected in human allergic bronchopulmonary aspergillosis. Allergen-induced cytokines are thought to regulate the inflammatory and immune responses in these animals. METHODS: In the present study, we exposed C57BL/6 and BALB/c mice to A. fumigatus antigen. Both wild-type and IL-4 knockout phenotypes of animals of both strains were used. Some animals were also treated with anti-IL-5 or anti-IFN-gamma. Total serum IgE, Aspergillus species IgG subclass, peripheral blood eosinophils, and lung histology were studied. RESULTS: The results demonstrate similar lung inflammation in all wild-type and IL-4-/- animals exposed to A. fumigatus antigen. Similarly, in spite of the diverse immune response produced by the anticytokine treatment, no major differences were detected among any of the animal groups studied. CONCLUSIONS: It can be concluded that A. fumigatus exposure in an immunologically unaltered host is predominantly of a Th2 type, and that depletion of the Th2 cytokine leads to a similar lung inflammation but with a characteristic Th1 response, suggesting that the pathogenesis of allergic aspergillosis is the result of multiple induction pathways.  相似文献   
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Physiological circadian rhythms are orchestrated by the hypothalamic suprachiasmatic nucleus (SCN). The activity of SCN cells is synchronised by environmental signals, including light information from retinal ganglion cells (RGCs). We recently described a population of vasopressin‐expressing RGCs (VP‐RGC) that send axonal projections to the SCN. To determine how these VP‐RGCs influence the activity of cells in the SCN, we used optogenetic tools to specifically activate their axon terminals within the SCN. Rats were intravitreally injected with a recombinant adeno‐associated virus to express the channelrhodopsin‐2 and the red fluorescent protein mCherry under the vasopressin promoter (VP‐ChR2mCherry). In vitro recordings in acute brain slices showed that approximately 30% of ventrolateral SCN cells responded to optogenetic stimulation with an increase in firing rate that progressively increased during the first 200 seconds of stimulation and which persisted after the end of stimulation. Finally, application of a vasopressin V1A receptor antagonist dampened the response to optogenetic stimulation. Our data suggest that optogenetic stimulation of VP‐RGC axons within the SCN influences the activity of SCN cells in a vasopressin‐dependent manner.  相似文献   
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