Biomedical subjects
Publications and source records attributed to E Garaci.
Prostaglandins of the A series strongly inhibit the production of Sendai virus in African green monkey kidney cells and are able to prevent the establishment of persistent infection ("carrier" state). This action is specific for prostaglandin A and is not due to alteration in the host cell metabolism or in the virus infectivity. The possibility that this effect is mediated by interferon is discussed.
This study evaluated the effects of PGA1 on B-16 melanoma-bearing mice. Intraperitoneal injection of PGA1 (10 microgram/day) significantly inhibited the rate of melanoma growth measured both as delay in the rate of appearance and decrease in the tumor volume. In contrast to the diluent control-treated mice, by 17 days, less than half of the PGA1-treated animals developed measurable (greater than 2 mm) subcutaneous tumors. In addition to its effect on tumor size, PGA1 was also effective in stimulating both the humoral and cellular components of the immune response. B-16 tumor-bearing mice were shown to be immunosuppressed, in that they had decreased anti-sRBC hemagglutinin titers, decreased splenic plaque-forming cells, suppressed delayed hypersensitivity responses, and delayed rejection of skin allografts from BALB/c mice. Although, PGA1 had relatively little effect on normal mice, this prostaglandin substantially improved all these immunologic parameters in tumor-bearing animals.
This study was performed to correlate the role of exogenous and endogenous prostaglandins on humoral and cellular immune responses to and rate of growth of B-16 melanoma in vivo. B-16 melanomas synthesized 7 times as much PGE as did adjacent normal tissues, an effect that was abolished by indomethacin. In C57BL/6J mice bearing B-16 melanomas splenic plaque-forming cells, hemagglutinin titers, and delayed hypersensitivity (all to SRBC) were profoundly suppressed; these responses were significantly augmented by treating the mice with di-M-PGE2 (16, 16-dimethyl-PGE2-methyl ester), a long acting analogue of PGE2, and either further suppressed or unaffected by indomethacin, a potent inhibitor of endogenous PGE biosynthesis. Compared to control experiments, indomethacin hastened the rate of development of palpable subcutaneous B-16 tumors and facilitated the proliferation of these cells in solid tumors as well as in ascites. Pretreatment of mice with di-M-PGE2 (before inoculation with tumor cells) resulted in delay in the rate of appearance of tumors, decline in the growth rate, and increased survival. These data suggest that prostaglandins are involved in the control of in vivo tumor cell growth largely by virtue of their effects on the immune response.
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Serum thymic factor (STF) activity was assayed in 26 young asthmatic patients and in 20 age-and sex-matched controls, in view of the increasing importance attributed to this thymic product in regulating several immune mechanisms. Determinations of total and specific IgE and of other immunoglobulins and skin tests were also performed. Decreased STF activity and high total and specific IgE concentrations were observed in the majority of asthmatic patients. In controls, STF activity was within normal limits in all cases and total and specific IgE concentrations were increased only on one case. The decreased STF activity may be responsible for a possible impairment of cell-mediated immunity and for the increased stimulation of the reaginic system observed in asthmatic patients, via its effects on some T cell subpopulation, namely, suppressor T lymphocytes, which seem particularly sensitive to STF variations. On the basis of these data and of the results of our study, a possible, although speculative, correlation between reduced STF activity and high IgE concentrations in asthmatic patients may be postulated. The reported increased occurrence of autoimmune phenomena in asthmatic patients is in agreement with the hypothesis of a STF-mediated suppressor T-lymphocyte quantitative and/or qualitative defect in this disease.
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Attempts at improving chemical fixation for electron-microscopic observation of the capsule of Klebsiella pneumoniae were made. The capsule was preserved by using alcian blue - lanthanum and tris-(1-aziridinyl) phosphine oxide (TAPO) - aldehyde - osmium procedures. Despite the different retention of the overall capsular material and minor variations in morphological details, in both cases the interpretation of ultrastructural patterns suggested that the capsule be composed of a meshed network of thin polysaccharide fibrils radiating from the cell wall. This organization is in keeping with all recognized chemical properties of bacterial polysaccharide capsules or, at least, does not contradict them. Moreover, an effective preservation of bacterial structures other than capsule has been obtained, mostly in specimens fixed by the TAPO-aldehyde-osmium method, a fact which gives further reliability to the technical approach used for capsule visualization.
Morphometric parameters of mitochondria such as volumetric density, surface density of envelopes and cristae and numerical density were calculated for control untreated and triacetyloleandomycin (TAO)-treated rat hepatocytes using a point-counting technique. Moreover, morphometric parameters calculated experimentally and those computed on the basis of the least square interpolation and the agreement with the chi2 test, were compared. The equations modelling each main morphometric parameter of experimental motochondria were also computed. Morphometric study revealed that TAO produces a highly reproducible pattern of morphological alterations in the mitochondrial population of rat hepatocytes, and a good agreement between experimental and theoretical data was found. The response of hepatocyte mitochondria to TAO may be modelled by parabolic functions described by equations of the second degree. During the whole experimental period, the number of mitochondria decreases, but the specific volume of mitochondria increases. The area of the cristae surface per mitochondrion does not change substantially during the whole experimental period but since the quantity of internal mitochondrial membranes per hepatocyte is less in the later experimental period than in control material, it can be assumed that the oxidizing capacity per hepatocyte has diminished. The morphometric model based on TAO-treated hepatocyte mitochondria is different from those so far described in the literature for rat liver.
Swiss mice treated with an antithymic reticuloepithelial cells serum (ATRES) showed a drastic and prolonged depression of the serum thymic factor. A similar but less pronounced effect was also observed following the administration of the antithymocyte (ATS) and the antilymphocyte (ALS) sera. Conversely, the azathioprine sensitivity of spleen spontaneous rosette-forming cells was highly modified by the ATRES but not by the ATS or the ALS. The probable mechanisms of such effects are discussed.
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