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Biomedical subjects

P Basse

Publications and source records attributed to P Basse.

29 records · Page 2Linked to original sources
PubMed1991

Multiple symmetric lipomatosis.

Multiple symmetric lipomatosis (MSL) is a rare disorder only mentioned in about 200 cases in the medical literature. It manifests as massive lipomatous deposits in specific areas of the body. The cause is unknown, although there frequently is a history of alcoholism. Surgical lipectomy has so far been the choice of treatment. We present a review of the disease and report one case successfully treated with liposuction.

Humans↗
PubMed1990

Comparison between 125IUdR and 51Cr as cell labels in investigations of tumor cell migration.

YAC-1 tumor cells double-labeled with Na2[51Cr]O4 [51Cr] and [125I]iododeoxyuridine [125IUdR] were injected intravenously into Balb/c mice in order to investigate their migration and fate 0-4 h after the injection. Whereas the clearance of tumor cells from the lung tissue was similar as judged with both labels, the kinetics of isotope uptake in the liver were strikingly different. Thus, retention of 51Cr in the liver was very high compared to a much lower and only transient retention of 125I. A higher retention of non-tumor cell-associated 51Cr was also observed in most other organs, resulting in overestimation of the number of viable tumor cells in these organs. Moreover, a marked spontaneous release (greater than 10% after 12 h) makes 51Cr less suitable as a cell label than 125IUdR. On the other hand, we found that the release of 125I from dead cells in vivo depends at least partially on host factors such as macrophages. Consequently, caution must be exerted when tumor cell migration is investigated in animals treated with drugs that might affect the reticuloendothelial system. We conclude that 125IUdR is superior to 51Cr as a cell label for investigation of tumor cell migration in vivo, even though some doubt about the reliability of the number of tumor cells in liver and carcass, predicted by this radiolabel, still remains.

Animals↗
PubMed1988

Fate of tumor cells injected into left ventricle of heart in BALB/c mice: role of natural killer cells.

The arrest, retention, and elimination (i.e., clearance) of radiolabeled YAC-1 lymphoma cells injected either iv or into the left ventricle (LV) of the heart were studied in male BALB/c mice, with special emphasis on the role of natural killer (NK) cells. After iv injection YAC-1 cells were arrested and, to a large extent, destroyed in the lungs, which contain the first capillary bed that iv injected tumor cells meet. After LV injection the initial distribution of the tumor cells, which depends on the distribution of cardiac output at the time of injection, was estimated by use of radiolabeled microspheres. Using this technique, we have shown that LV-injected tumor cells, in contrast to iv injected tumor cells, were not arrested in the first capillary bed that they encountered but passed viably through the microvasculature of the brain, heart, kidneys, intestinal tract, and to some extent, the bone, skin, and muscle. The only organs that could arrest the LV-injected tumor cells were the lungs and the liver. In the lungs clearance of YAC-1 cells began immediately after the cells were arrested. However, the rate of clearance could be almost abrogated by pretreatment of the recipients with anti-asialo GM1 antiserum, which destroys most of the NK cells in vivo and strongly depresses the in vitro NK cell activity. In contrast, YAC-1 cells arrested in the liver were not cleared from this organ during the first 1-2 hours after arrest. After this delay clearance of the cells commenced. Pretreatment of the recipients with anti-asialo GM1 also strongly depressed the clearance of tumor cells from the liver. Although pretreatment with polyinosinic-polycytidylic acid enhanced in vitro NK cell activity, it could augment only slightly the clearance of YAC-1 cells from the lungs and the liver. Thus these results strongly support the hypothesis that the rapid clearance of tumor cells from both the lungs and the liver depends, at least partially, on the NK cell activity within these organs.

Animals↗
PubMed1988

IFN-induced modulation of histocompatibility antigens on human cells. Background, mechanisms and perspectives.

IFN proteins are a family of lymphokines with anti-viral effects. Several other effects of IFNs have also been described, including enhancement of natural killer (NK) cell activity, enhancement of cytotoxic T-lymphocyte activity, and enhancement of the expression of major histocompatibility complex (MHC) antigens. The latter effects have been characterized as immunomodulatory, whereas the well-known inhibition of growth of malignant cells has been termed anti-proliferative. This review summarizes the current knowledge of the enhancement of MHC products by IFNs. Whereas the basic methodologies for demonstrating the enhancement are simple and reliable, especially when using flow cytometry (FCM), the biological relevance of this reaction is largely unknown. Based on recent findings, however, we have hypothesized that the above-mentioned diverse effects of IFNs are all - in some way or other - related to the classical anti-viral mechanism. This concept proposes that the MHC-enhancing effect of IFNs is a vital part of the immunological defense against virus infections and an integral part of the anti-viral effects of IFN proteins.

Antiviral Agents↗
PubMedDate not supplied

Endogenous and adoptively transferred A-NK and T-LAK cells continuously accumulate within murine metastases up to 48 h after inoculation.

In murine models, therapeutic efficacy of adoptive immunotherapy (AIT) of cancer with lymphokine activated killer (LAK) cells is seen only when applied together with substantial doses of interleukin-2 (IL-2), probably because this cytokine is imperative for both motility and viability of the LAK cells. We wanted to investigate whether IL-2 in addition mediates an immunostimulatory activation and expansion of endogenous effector cells contributing to tumor regression. Using an immunoperoxidase technique, we have been able to longitudinally analyze the accumulation of tumor infiltrating lymphocytes expressing the pan-T cell/activated lymphocyte phenotype (Thy1.2), the natural killer (NK) cell phenotype (AsGM,) as well as the cytotoxic T (CD8) cell phenotype within experimental established B16 pulmonary melanoma metastases in C57BL/6 mice during the first 48 h after high dose IL-2 monotherapy. Whereas a substantial and selective infiltration of AsGM1+ lymphocytes in tumor tissue was seen (262 and 937 cells per sq.mm malignant tissue at 0 and 48 h, respectively), only a minor increase in accumulation of CD8+ cells was seen (106 and 171 cells per sq.mm tumor tissue at 0 and 48 h, respectively). The addition of adoptive transfer with lymphokine-activated adherent NK (A-NK) cells to the high-dose IL-2 treatment resulted in more than a 1.5 fold increase in infiltrating AsGM1+ cells compared to IL-2 therapy alone (1520 compared to 937 AsGM1+ cells per sq.mm malignant tissue). No substantial accumulation of CD8+ cells was observed in this setting either. In contrast, the treatment with high dose IL-2 together with adoptive transfer of mitogen-stimulated, lymphokine-activated T killer (T-LAK) cells increased the infiltration of CD8+ cells 10-fold compared to IL-2 monotherapy (2078 compared to 171 CD8+ cells per sq.mm malignant tissue, respectively). Interestingly, infiltration of both endogenous and exogenous cells continued over time, since the effector-to-tumor cell ratio in metastatic tissue dramatically increased from 1:8 and 1:6 at 16 h to 1:3 and 1:2 at 48 h after adoptive transfer of A-NK and T-LAK cells, respectively. These data underline the longevity of LAK cells in vivo and highlight the importance of IL-2 treatment in recruiting endogenous immune cells to tumor areas.

Adjuvants, Immunologic↗
PubMedDate not supplied

Morphological studies of effector cell-microvessel interactions in adoptive immunotherapy in tumor-bearing animals.

Murine lymphokine-activated natural killer (A-NK) cells are able to migrate to and accumulate in tumor metastases. However, the exact migratory pattern is as yet unknown. In the present study, we have investigated the migration from the vasculature towards malignant tissues of various effector cells. Our results indicate that murine A-NK cells seem to be arrested for an extended period of time in the microvasculature and also, although infrequently, to adhere to the endothelial lining of larger vessels close to tumor tissues before extravasation. While murine T lymphokine-activated killer and rat A-NK cells accumulate significantly in the subendothelial areas of larger venules in normal tissues, no such accumulation is observed with respect to murine A-NK cells. Electron microscopy reveals that the murine A-NK cells undergo an extreme deformation during extravasation and tumor infiltration. Furthermore, the cells are shown to be in an activated stage probably facilitating their migration, and hence, the elimination of tumor cells.

Adenocarcinoma↗