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Biomedical subjects

G Biasi

Publications and source records attributed to G Biasi.

At least 19 recordsLinked to original sources
PubMed1979

Lack of T-cell mediated cytotoxicity in M-MSV system depending on H-2 haplotypes.

The H-2 restriction phenomenon was evaluated with regard to the immune response to Moloney sarcoma virus (M-MSV)-induced tumours in the mouse. Using an in vitro 51Cr release assay the lytic activity of lymphocytes from M-MSV immune strains of mice, including several H-2 recombinant strains, was determined on leukaemic cell lines originally induced in mice of different strains by neonatal infection with Moloney leukaemia virus. In analogy with other experimental models, it was observed that a compatibility between effector and target cells at the K and/or D regions is generally necessary and sufficient to obtain the cytotoxic effect. However, for the H-2d and H-2b haplotypes, identity at the K or D region respectively was not sufficient for lysis to occur. Attempts to demonstrate that this lack of activity might be associated with the absence of H-2 linked Ir responder genes, were not successful.

Animals↗
PubMed1978

The role of H-2 and H-2-like determinants in syngeneic and allogeneic cytostasis.

Specific sensitization against H-2 determinants was affected by immunizing allogeneic mice with spleen and lymph node cells in H-2 congenic combinations. Lymph nodes from the sensitized and non-sensitized mice were respectively cultured together with H-2 syngeneic tumour cell lines. The growth and viability of the tumour cells was subsequently measured by the amount of radiothymidine incorporation. If the tumour cells incorporated less isotope when cultured with the immune cells than with the normal cells this was termed 'cytostasis'. To identify the H-2 genes controlling the sensitization phase in the cytostasis assay, we studied the effect on different transplantable tumour target cells of lymphoid cells from mice sensitized against different congenic spleen cells. The results suggest that the cytostasis assay can can measure an in vitro specific response to H-2-incompatible sensitizing antigens, and that I--B incompatibility, together with K and/or D, is essential to produce effectors. Furthermore, H-2 allogeneic sensitization could induce cytostasis even against tumour cells syngeneic for the H-2 halotype of the responder strain. The implications of these findings are discussed.

Animals↗
PubMed1978

Secondary in vitro generation of cytolytic T-lymphocytes (CTL's) in the murine sarcoma virus system. Virus-specific CTL induction across the H-2 barrier.

Following in vitro stimulation of murine sarcoma virus Moloney isolate (M-MuSV)-immune spleen cells with syngeneic antigenically related Moloney leukemia cells, highly efficient cytotoxic T-lymphocytes (CTL's) were generated. The cytotoxic effect was directed only against H-2-compatible target cells bearing M-MuSV tumor-associated antigens (TAA). However, in a cold target competition assay a weak but detectable capacity to block CTL activity was also obtained when allogeneic Moloney leukemia cells were added. Moreover, when M-MuSV-immune spleen cells from mice inoculated with virus 14 days previously were stimulated by allogeneic Moloney leukemia cells, a strong cytotoxic effect toward syngeneic and allogeneic tumor cells bearing M-MuSV TAA was elicited.

Animals↗
PubMed1977

[The SITAR Project. A new approach to diagnosis and surgical indication in arteriopathic patients].

The extreme variations with which atherosclerotic disease presents as regards progression index, arterial bed localization frequency, malignity and invasiveness in different ages and often as regards different anatomopathological aspects characterizing the formation and course of the primary lesion, mean that there are still many unknowns in the aetiopathogenesis, diagnosis and operative indications for this disease. Such problems are more and more important to the vascular surgeon who, with the development of atherosclerotic disease, sees the long-term results of his arterial reconstructive surgery compromised. The vascular surgeon is therefore directly involved with his colleagues in the internal medicine and pharmacological departments in problems connected with the pathogenesis of arteriosclerosis, and indeed he contributes to setting new constraints on the choice of prosthetic materials, for use in cases of bridge-work, and in the creation of new surfaces by means of thrombendarteriectomy. On the basis of such considerations, the IInd Surgical Clinic of Milan University began, in 1975, a study whose end purpose was the drafting of a clinical card designed for data computerization. Compiled by the surgeon, it is intended essentially for vascular surgeons. However, as it is personally considered that by the very nature of the disease, the atherosclerosis approach must be interdisciplinary, it also concerns physicians in the internal medicine, pharmacological and dietological departments.

Arterial Occlusive Diseases↗
PubMed1977

Inhibitory effect of YC8 leukaemia cell line on in vitro lymphocyte reactivity.

Mitomycin-treated transplantable Moloney virus-induced lymphatic leukaemia cells (YC8) not only failed to stimulate normal allogeneic lymphocytes in one-way mixed leucocyte culture (MLC) but also exerted a strong inhibitory effect on the proliferative response of normal lymphocytes, in MLC and after stimulation by mitogens. Potentially inhibitory factors which could be released in the culture fluids by the YC8 cells were not found, but a YC8-derived adherent cell subpopulation was identified as being responsible for the in vitro suppression.

Animals↗
PubMed1976

Generation of cytotoxic cells in absence of blastogenesis by mouse leukemic cells in mixed cultures.

Primary virus-induced murine leukemias and transplantable leukemic cell lines, originally induced by virus, chemical or physical agents, failed to stimulate normal spleen cells differing at the H-2 complex or at Mls locus in the one-way mixed leukocyte culture. Lack of stimulation seems at least partially due to a nonspecific inhibitory effect since in a "three-party" culture system the leukemic cells interfered with the mixed leukocyte reaction (MLR) of normal allogeneic cells. Characterization of the leukemic cell populations used, according to their T or B cell origin, disclosed that in most cases T cell markers were present. Also, no Ia antigens were detected on leukemic cells. Furthermore, using a 51Cr release assay, leukemic cells could sensitize allogeneic normal lymphocytes to kill specifically normal as well as leukemic targets, even when no MLR was detected in parallel cultures.

Animals↗
PubMed1976

Immune reactivity in the Moloney strain of murine sarcoma virus oncogenesis: requirement of thymus-derived lymphocytes for in vivo protection.

To study the function of different lymphocyte populations in the Moloney strain of murine sarcoma virus (M-MuSV) tumorigenesis, we gave M-MuSV injections to CBA mice selectively deprived of thymus (T) lymphocytes by thymectomy, X-rradiation, and syngeneic bone marrow injection. Although no tumors appeared in the control group, 80% of the derived mice had tumors that grew progressively and ultimately killed them. In deprived mice, grafted with a syngeneic thymus (reconstituted mice) before or after an M-MuSV injection, tumors regressed or did not develop. Histologically, the lymph nodes and spleens of reconstituted mice, compared to those of deprived animals, showed repopulation of the thymus-dependent areas and prominent follicles in the cortex. Moreover, tumor tissue of reconstituted mice was extensively infiltrated by lymphocytes. To evaluate the number of lymphoid cells needed to prevent or regress M-MuSV tumors, we injected varying amounts of lymphoid cells into deprived mice. Even low lymphocyte numbers (10(6) cells) were sufficient to exert, in some cases, protection against M-MuSV tumorigenesis. This effect was not abolished by subsequent splenectomy or antilymphocyte serum treatment. Finally, deprived mice, given repeated injections of antiserum (hyperimmune) against M-MuSV, had tumors which appeared only after a prolonged latency. From these results, it is concluded that T-cell population integrity is important in affording total host protection against the M-MuSV tumors.

Animals↗
PubMed1975

Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. I. Genetics of resistance in AKR mice.

Infection of Moloney mouse sarcoma virus (M-MSV) in adult mice of several inbred strains revealed that all strains except AKR are highly susceptible to M-MSV tumor development. F1 hybrids between AKR and CBA, DBA/2 or NIH mice are as resistant (93%) as the parental AKR strain, which indicates that resistance is transmitted as a dominant character. First backcross mice to the susceptible parent show a 3:1 ratio of resistant to susceptible mice. This is the expected ratio for two segregating loci which independently confer resistance. The incidence of resistant F2 mice is somewhat lower than expected. Further support for the two-gene hypothesis was obtained in second backcross mice. None of the major genes affecting MuLV infection (Fv-2 and H-2) seems to play any role in this system and no linkage was found with Thy. 1 and albino, dilute, agouti and brown markers.

Animals↗
PubMed1975

Genetic control of oncogenesis by murine sarcoma virus Moloney pseudotype. II. A dominant epistatic susceptibility gene.

We have shown in the preceding paper that AKR mice are highly resistant to M-MSV tumor development, and that resistance is transmitted as a dominant character. In the present studies the tumor-response pattern of F1 hybrids between resistant AKR and susceptible strains (C57Bl/6, BALB/c and B10BR) following injection with Moloney mouse sarcoma virus (M-MSV) resembles that of the non-AKR parent. Segregation is observed in first backcross (Bc1) and F2 mice, and the segregation ratios up to Bc3 mice fit a one-gene model. The data of triple cross hybrids suggests that this dominant susceptibility gene inhibits the phenotypic expression of M-MSV tumor resistance in some susceptible Fv1bb strains as well as in their hybrids with AKR. Neither Fv-1 nor H-2 exerts any significant influence on this complex system.

Animals↗
PubMed1975

In vitro and in vivo evaluation of T and B lymphocyte functions in AKR mice.

To investigate whether AKR spontaneous leukaemogenesis is associated with a reduction in functional activity of T lymphocytes, the PHA response of AKR blood cells at different ages up to and including the preleukaemic period was studied. No significant differences were observed among young, adult and preleukaemic donors. In addition, the in vitro and in vivo AKR lymphocyte functions were compared with those of CBA lymphocytes by means of their response to stimulation with T and B lymphocyte selective mitogens (PHA, Con A and LSP respectively), and their response to immunization with thymus dependent (SRBC) or independent (LPS) antigens. We observed in vitro that while the B lymphocytes responded normally to mitogen, an intrinsic hyporeactivity to mitogens characterizes the T lymphocytes. Moreover, AKR mice exhibited a reduced in vivo response to both thymus dependent and independent antigens.

Age Factors↗
PubMed1975

In vivo interactions between murine leukemia and sarcoma viruses.

Experiments have been performed with the aim of elucidating the nature and the extent of the in vivo interactions between murine leukemia viruses (MuLVs) and murine sarcoma virus (MSV). BALB/c and CBA mice, injected neonatally with Graffi or passage A Gross viruses (MuLV-Gi, MuLV-G), have been inoculated as young adults with murine sarcoma virus, Moloney strain (MSV-M). A higher percentage of nonregressing sarcomas appeared in these animals, sometimes accompanied simultaneously by leukemia. The immune reactivity of mice receiving MuLV-Gi at birth was found to be significantly depressed when evaluated by the hemolytic palque-forming cell (PFC) technique. However, in mice infected with MuLV-Gi and MSV-M the number of PFC ranged within the control values or slightly increased. The potentiation of MSV-M oncogenicity following infection with MuLV was studied in a more natural situation. Adult AKR mice, known to release endogenous MuLV continuously, were injected with MSV-M. The incidence of induced sarcomas was similar to that observed in control BALB/c mice inoculated with MSV-M. Moreover, tumors developed with a very long latent period. On the other hand, the great majority of tumors showed no regression and ultimately killed the host. Additional experiments, making use of immunologic manipulation of the host and Fl hybrids, suggest that the relative resistance to MSV-M oncogenesis in AKR mice is influenced by genetic and immunologic factors. MSV recovered from MSV-M-induced tumors in AKR and C58 mice was typed by highly specific mouse antisera. The results clearly showed that formation of a new MSV pseudotype occurred in vivo, the endogenous Gross virus acting as helper.

AKR murine leukemia virus↗
PubMedDate not supplied

Kinetics of insulin secretion following glucose infusion in patients with atherosclerotic peripheral vascular disease.

Kinetics of insulin secretion following an i.v. glucose infusion, according to the protocol described by Cerasi and Luft, were studied in 19 patients with angiographically documented atherosclerotic peripheral vascular disease and in a group of appropriate controls without clinical signs of disease. No significant differences were noted between patients and controls in plasma cholesterol levels and in the K value following a standard i.v. glucose tolerance test. Blood glucose levels were significantly lower in the patients, whereas mean plasma insulin and triglyceride levels were significantly higher. Analysis of the glucose and insulin responses to the glucose infusion test indicated that 31.6% of the patients had a delayed and sluggish insulin response to the glucose load, fitting the criteria suggested for the diagnosis of prediabetes, versus 10% of the appropriate controls. In particular, simulation of the plasma insulin responses by a square-wave glucose stimulus, confirmed that in a significantly higher number of patients the early insulin peak was below normal limits. The results of this study suggest that increased insulin secretion is not present in patients with atherosclerotic vascular disease, in contrast to reports by other authors, and that inefficient insulin secretory mechanisms may be observed in these patients, thus possibly contributing to the development of the atherosclerotic disease.

Adult↗