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Biomedical subjects

R Evans

Publications and source records attributed to R Evans.

At least 361 records · Page 20Linked to original sources
PubMed1985

Heredopathia atactica polyneuritiformis: Refsum's disease.

Seven patients with Heredopathia Atactica Polyneuritiformis are described. There were 3 groups of clinical characteristics: first, congenital abnormalities such as skeletal deformities, unrelated to phytanic acid levels; second, signs and symptoms such as retinitis pigmentosa which come on slowly and are not directly related to the plasma phytanic acid level; third, lesions such as the neuropathy, rash and cardiac arrhythmias which can change quickly and are linked to the plasma phytanic acid level. Exacerbations of the signs in the third group are precipitated by a low calorie intake and mobilisation of phytanic acid from the adipose tissue. Poor vision is due not only to retinitis but also to small pupils which fail to dilate in the dark. The use of plasma exchange is discussed. With good dietary supervision it is possible to produce a considerable clinical recovery for the neuropathy.

Adipose Tissue↗
PubMed1985

Penetrating injuries: how easy is it to see glass (and plastic) on radiographs?

The radiopacity of objects commonly associated with penetrating wounds and made from modern glass was assessed. It is concluded that all glass fragments should be detected because they are all radiopaque. Occasionally thin slivers of glass may be difficult to detect, but should be visualised with good radiography and careful scrutiny. Plastic from the housing of motor vehicle lamps is not radiopaque.

Foreign Bodies↗
PubMed1985

Measurement of lumbar spine bone mineral: a comparison of dual photon absorptiometry and computed tomography.

A comparison of computed tomography (CT) and dual photon absorptiometry (DPA) in the measurement of spinal bone mineral was made in 44 subjects of whom 26 had vertebral crush fractures. Although CT measures only trabecular bone within the vertebral body whilst DPA measures the whole vertebral segment, a good correlation was observed (r = 0.80) when these quantities were expressed in dimensionally similar units. Trabecular bone in the distal radius measured by CT correlated less well with vertebral CT (r = 0.65). Cortical bone in the radius correlated poorly with the spinal DPA measurement (r = 0.38).

Adult↗
PubMed1985

The immunological basis of tumor rejection: the absolute dependence of the effector arm on sensitized T cells after chemoimmunotherapy of a murine sarcoma.

The mechanisms of tumor rejection were investigated by using a therapeutic model system involving treatment of C57BL/6J (B6) mice bearing the syngeneic MCA/76-9 or the unrelated MCA/76-64 sarcomas with cytoxan and tumor-sensitized T lymphocytes. Separated tumor-associated T lymphocytes (TAL) and tumor-associated macrophages (TAM) isolated from the regressing tumors 8 to 10 days after combination therapy expressed relatively specific cytotoxicity in vitro, whereas the unseparated tumor-associated cells (TAC), consisting of a mixture of TAL and TAM, expressed nonspecific cytotoxicity. TAM-mediated cytotoxicity was not dependent on the presence of TAL, as shown by T cell depletion of TAM or TAC cultures with the use of monoclonal anti-Thy-1 or anti-Lyt-2 antibody and complement. In contrast, the nonspecific cytotoxicity was dependent on the presence of T cells. In vivo assays using the Winn test failed to confirm certain aspects of the in vitro data. Without exception, the TAC inhibited tumor growth in an immunologically specific manner, having no effect on the growth of the unrelated B6 sarcoma. T cell depletion completely abrogated in vivo cytotoxicity. Specificity of tumor growth inhibition was confirmed in a bystander experiment in which TAC were mixed with both tumor cell types and were injected into recipient B6 mice. Tumors grew under these conditions, but the tumor that grew consisted only of those tumor cells toward which TAC cytotoxicity was not specifically directed. A bioassay indicated that the specifically immune antitumor effects at the site of regression were initiated between days 3 and 7 after combination therapy. By days 7 and 9, few tumorigenic stem cells could be detected at the tumor site. However, T cell depletion of the TAC isolated on days 8 to 10 resulted in enhanced tumor growth when the depleted TAC were injected into recipient mice. The conclusions reached were that tumor rejection was absolutely dependent on T cell participation at the tumor site, and that if TAM were involved, they required the presence of TAL and did not express nonspecific antitumor cytotoxicity. Indeed, the accelerated tumor growth seen in the absence of TAL suggested the possibility that TAM were growth stimulatory.

Animals↗
PubMed1985

Amplification of immune T lymphocyte function in situ: the identification of active components of the immunologic network during tumor rejection.

Previous data had indicated that sarcoma-bearing mice receiving combination therapy consisting of a single i.p. injection of cytoxan (CY) and an i.v. injection of tumor-sensitized T cells (immune cells) rejected the neoplasm. The reaction was immunologically specific and dependent on donor T cells. This report is concerned with the hypothesis that the transfer of immune cells results in the amplification of T cell responses at the tumor site. Using C57BL/6J mice bearing the syngeneic rhabdomyosarcoma MCA/76-9, we show that 6 to 9 days after combination therapy those components usually associated with the immunologic network were present at the tumor site. Tumor-associated macrophages (TAM) and lymphocytes (TAL) were shown to produce IL 1 and IL 2, respectively. The TAM expressed Ir gene products (Ia) and were able to present the synthetic polymer GAT to specifically sensitized lymphocytes. In addition, it was demonstrated by in situ labeling with 3H-TdR that lymphocytes associated with the regressing tumors were proliferating. The peak incorporation occurred 7 days after therapy, 24 hr before a significant increase in the T cell content of the tumors. The data indicate that those facets of the immunologic network necessary for amplification were present at the site of rejection.

Animals↗
PubMed1984

Tumor-associated macrophages stimulate the proliferation of murine tumor cells surviving treatment with the oncolytic cyclophosphamide analogue Asta Z-7557: in vivo implications.

This report is concerned with the hypothesis that tumor-associated macrophages (TAM) present during cyclophosphamide (CY)-induced tumor regression stimulate proliferation of tumor stem cells that remain after the oncolytic after of CY has dissipated. In preliminary studies, plasma or serum from CY-injected mice was used as a source of CY metabolites. However, because of the relatively high background toxicity of normal mouse plasma/serum and the lack of a precise technique to quantify how much metabolite was present at any one time, this approach was abandoned. In place of the plasma metabolites, we used the Cy analogue, 4-(2-sulfonatoethylthio)-cyclophosphamide cyclohexylamine salt, Asta Z-7557. On solubilization in water, Asta Z-7557 yields phosphoramide mustard, one of the oncolytic metabolites of CY in vivo. This approach enabled us to quantitate the amount of drug used in vitro and to control the amount to which tumor cells and macrophages were exposed. It was demonstrated that when two different C57BL/6J tumor cell targets, the MCA/76-9 sarcoma and the EL4 lymphoma subline, E2G.2, were treated with defined quantities of Asta Z-7557, those cells surviving the toxic effects were stimulated to proliferate in the presence of TAM isolated from the MCA/76-9 sarcoma. Although pretreatment of the TAM with the drug slightly diminished the stimulatory effect, this was still significantly greater than the effect of culture medium alone. In no instance was there evidence that drug treatment rendered the macrophages cytotoxic towards the tumor cells. The data supported the notion that in vivo the presence of a high proportion of TAM during CY-induced temporary tumor regression may contribute directly to the resurgence of tumor growth.

Animals↗
PubMed1984

Distribution of tumor-sensitized cells during the induction of permanent tumor regression by chemoimmunotherapy: the use of glucose phosphate isomerase as a marker.

Using a previously described tumor model system, in which permanent tumor eradication was induced by treatment with cyclophosphamide (CY) and adoptively transferred tumor-sensitized (immune) spleen cells, we determined the distribution of the transferred cells in recipient mice. The experiments were carried out using the C57BL/6J (B6) sarcoma, MCA/76-9, and B6 and congeneic B6.CAST.Gpi-Ia strains, which are homozygous for the glucose phosphate isomerase (Gpi) alleles Ib and Ia respectively. Thus, tumor-bearing mice of the one strain were injected with CY (200 mg/kg) 10 days after implantation of tumor cells and 4 h later with an intravenous injection of 50 X 10(6) immune cells from presensitized mice of the other strain. It was observed that the donor-type isozyme was expressed in the tumor within 24 h of injection and continuously up to the time at which the tumor mass had totally regressed (11 days). The tumor-associated macrophage and neutrophil fractions were shown to express host-type isozyme, while the lymphocyte fraction expressed isozyme of both host and donor type. The donor-type isozyme did not appear in the blood until day 4 but persisted thereafter for long periods. The spleen and lymph nodes expressed donor-type isozyme by 1 day after chemoimmunotherapy and remained positive for the duration of the experiments. The adoptive transfer of normal (non-immune) spleen cells gave similar results, except that donor-type isozyme did not persist at the tumor site. The conclusion reached was that the injection of either normal or immune donor spleen cells after CY treatment of B6 mice gave rise to chimeric mice, in which the distribution of normal and immune donor cells was basically similar in terms of overall isozyme expression. However, only immune donor cells resulted in the appearance of both donor and host T cells at the tumor site, suggesting amplification of both donor and host lymphocyte function either at the tumor site or in the lymphoid tissues.

Alleles↗
PubMed1984

Phenotypes associated with tumor rejection mediated by cyclophosphamide and syngeneic tumor-sensitized T lymphocytes: potential mechanisms of action.

The phenotypes of the affector and effector cell populations involved during the induction of permanent tumor regression by combined therapy using cyclophosphamide (CY) and immune spleen cells were identified. Permanent tumor regression was dependent on the presence of Thyl+ Lyt-2+ lymphocytes in the immune spleen cell population that was injected i.v. 2-4 h after an intraperitoneal injection of CY (240 mg/kg) into C57BL/6J mice bearing 1.0-1.5 g. MCA/76-9 or MCA/76-64 sarcomas. Histological evaluation after the combined treatment indicated an intense influx of putative lymphocytes 6-10 days after the combined treatment, over and above the inflammatory response involving macrophages and neutrophils induced by CY treatment alone. These infiltrating cells were shown to be T lymphocytes, most of them having the Lyt-1 and Lyt-2 antigens on their cell membrane. Isolated MCA/76-9 or 76-64 tumor-associated cells (TAC), lymphocytes (TAL) and macrophages (TAM) inhibited MCA/76-9 or 76-64 tumor growth respectively in a Winn test in an immunologically specific manner, having no effect on the growth of the B6 sarcoma cells, MCA/76-45 and 77-23. The tumor-free mice from the Winn test were not resistant to a subsequent challenge inoculum of either MCA/76-9 or 76-64 cells. Isolated TAC were usually non-specifically cytotoxic in vitro, while TAL and TAM showed some degree of specificity. The overall data indicated that the ultimate rejection of those tumor cells remaining after the direct anti-tumor action of CY had been dissipated was probably mediated by the combined action of TAL and TAM.

Animals↗
PubMed1984

Regulation of T- and B lymphocyte responses to mitogens by tumor-associated macrophages: the dependency on the stage of tumor growth.

This preliminary investigation was concerned with the hypothesis that macrophages associated with tumors induced to regress temporarily by the action of cyclophosphamide (CY) have the capacity to suppress local T- or B lymphocyte responses which otherwise might cause permanent regression. Cultures of adherent cells, predominantly tumor-associated macrophages ( TAMs ), isolated from two C57BL/6J (B6) sarcomas, MCA/76-9 and 76-64, after various periods of tumor growth or after CY injection (240 mg/kg) were shown to suppress or enhance the response of 10(6) B6 normal spleen cells to stimulation by concanavalin-A (Con A) or lipopolysaccharide (LPS). At any given time point, the extent of suppression or enhancement induced by adherent cells isolated from tumors after CY injection was similar to that induced by cells from progressing tumors and appeared to be more dependent on the time after the initial injection of tumor cells than on drug treatment per se. Thus, adherent cells suppressed Con A and LPS responses when they were isolated either from small (0.5 g) or large (greater than 1.5 g) progressing tumors or from tumors 4-9 days after CY injection. However, during the logarithmic phase of tumor growth or within 4 days of injecting CY, adherent cells enhanced spleen cell mitogenic responses, particularly to LPS stimulation. The cultures of putative TAMs isolated at the various time points were seen to contain varying proportions of polymorphonuclear cells (PMNs), the proportions coinciding with the period of reduced spleen cell mitogenic responses. Cultures prepared from small or large progressing tumors contained about 10% or 20-30% PMNs, respectively, while those from tumors tested during the log phase contained less than 5% PMNs. Cultures from tumors removed within 4 days of injecting CY contained less than 5% PMNs while those prepared from tumors tested at later times contained as high as 25% PMNs by 9 days after CY injection. A comparison of peritoneal PMNs and macrophages from non-tumor-bearing mice in terms of their ability to influence mitogenesis indicated that PMNs at high ratios (1 PMN:2 spleen cells) could suppress responses directly. Lower ratios had either small suppressive effects or no effects but in no case was enhancement of responses seen. Peritoneal macrophages suppressed responses at a ratio of 1 macrophage:10 spleen cells but enhanced responses at ratios of 1 macrophage:100 or 1,000 spleen cells. The overall data indicated that the microenvironment of the tumor site may modulate the functional activity of macrophages, or their subpopulations, during their potential regulation of T- and B-cell responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

In situ proliferation of intratumor macrophages.

This investigation was carried out to assess whether the progressive increase in the number of macrophages associated with growing tumors was the result of an influx of monocytes from the circulation as well as proliferation of macrophages in situ. Tumor-associated macrophages (TAM) were identified in cell suspensions prepared from three C57BL/6J (B6), methylcholanthrene-induced sarcomas, designated MCA/76-9, 76-64, and 77-23, growing in normal or irradiated mice. When the sarcomas were implanted in B6 mice exposed to a sublethal dose (800 R) of whole body irradiation ( WBI ), tumors grew very slowly compared with control tumors. The TAM numbers were small and the percentages of macrophages were very low. The levels of TAM corresponded with the low number of circulating blood monocytes. However, compared with the number of TAM in the initial inoculum of tumor cells injected into the WBI or control mice, the TAM numbers over a period of 14 days increased several fold in WBI mice. That this increase was initially due to infiltration from the circulation was shown by injecting macrophage-free, cultured tumor cells into WBI or control mice. Proliferation in situ was demonstrated by autoradiography experiments. When 3H-thymidine was injected 1 hr before excision of MCA/76-9 tumors, labeled cells were seen in histological sections and in cell suspensions. The labeling indices for TAM from tumors growing in WBI or normal mice were not significantly different from tumor cell labeling indices. The overall data indicated that the progressive increase in TAM in these sarcomas was the combined result of monocyte infiltration and proliferation of macrophages in situ.

Animals↗
PubMed1984

The management of cardiac tamponade in patients with breast cancer.

Six patients with disseminated breast cancer and cardiac tamponade were treated with a pleuropericardial window and in four patients with systemic chemotherapy. The median survival of these six patients was 17 months (range 1-50 months). These results indicate that aggressive therapy in patients with cardiac tamponade and breast cancer can lead to prolonged survivals.

Aged↗
PubMed1984

Macrophage-mediated cytotoxicity against cultured pancreatic islet cells.

Direct macrophage cytotoxicity against islet cells was examined in a morphological and biochemical study using mouse pancreatic islet cell monolayers cultured in the presence of macrophages. Secretory responsiveness of CBA/J beta cells was tested after 4 days of coculture with syngeneic or allogeneic (C57BL/6J) peritoneal macrophages. Although basal secretion of insulin in response to 5.5 mM glucose was not affected, stimulated insulin secretion in response to 16.5 mM glucose and 5 mM theophylline was reduced by as much as 70% in the presence of syngeneic or allogeneic macrophages. No such effect on stimulated insulin release was observed from cultured islets incubated in the presence of macrophage-conditioned medium. After refeeding the cultures at 4 days, zones of islet cell lysis began to appear wherever macrophages came into contact with islet cells. This macrophage-mediated killing was observed regardless of the source of the macrophages (e.g., intraislet "resident" macrophages, thioglycollate-stimulated peritoneal exudate macrophages, bone-marrow-derived macrophages, and splenic macrophages). The killing was seen with both syngeneic and allogeneic macrophages. Macrophages adjacent to islet cells extended filopodia into the monolayers, and those that adhered to the top of the islet cells formed lytic plaques. This study, by providing direct evidence of macrophage cell-mediated killing of islet cells, suggests the value of eliminating resident macrophages prior to islet transplantation into syngeneic or allogeneic hosts.

Animals↗
PubMed1984

Spontaneous and induced leukemias of myeloid origin in recombinant inbred BXH mice.

BXH-2 recombinant inbred (RI) mice produce high titers of B-ecotropic murine leukemia virus beginning early in life and have a high incidence of non-T-cell leukemias that occur before 1 year of age. The leukemias that develop are in some cases associated with hind limb paralysis. In addition, a dualtropic mink cell focus-forming virus has been isolated from leukemic cells of BXH-2 mice. Immunological and cytochemical characterization of the BXH-2 leukemias showed that they are of the myeloid lineage. To assess the oncogenicity of the BXH-2 viruses, newborn mice of several BXH RI strains were inoculated at birth with biologically cloned B-ecotropic or mink cell focus-forming murine leukemia virus. These studies demonstrated that the B-ecotropic virus can induce myeloid leukemias in other BXH RI strains, whereas the dualtropic mink cell focus-forming isolates were nononcogenic in the strains tested. DNA-DNA reassociation analysis indicated that the organotropism of the B-ecotropic murine leukemia virus is confined to lymphoid tissues. Southern analysis of tumor DNAs showed that there was amplification of ecotropic virus-specific sequences in BXH-2 myeloid tumors and in all leukemias induced in other BXH RI strains by inoculation of the BXH-2 B-ecotropic virus. Although B-ecotropic virus is expressed in central nervous tissues of paralyzed BXH-2 mice, we were unable to induce the disorder in several BXH RI strains inoculated intracranially at birth with either the B-ecotropic or dualtropic virus. These results suggest that the paralysis that occurs in BXH-2 mice is due to the infiltration of leukemic cells into the central nervous system.

Animals↗
PubMed1984

Anaemia in cats.

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Anemia↗
PubMed1984

A comparative study of dialysis techniques.

Comparative studies were performed on 19 patients who were dialysed initially for a mean of 25 h a week and then for a mean of 11.1 h a week over two 3-year periods. Clinical, biochemical, haematological and neurological valuations were performed, which showed no significant difference. As an adjunct to haemodialysis a perfusion system was added to 12 of these patients already stable on haemodialysis and estimations made of removal of middle molecular weight substances from plasma by a gel filtration method through a Sephadex column. The results of these various techniques are reported and the comparisons between haemodialysis, haemodialysis and ultrafiltration and haemodialysis, perfusion and ultrafiltration are given.

Blood↗