Search PubMed⌕ Search

Biomedical subjects

M Dietz

Publications and source records attributed to M Dietz.

At least 55 records · Page 3Linked to original sources
PubMed1979

Spontaneous regression of Friend murine leukemia virus-induced erythroleukemia. IV. Effects of radiation and athymia on leukemia regression in mice.

The spontaneous regression of the erythroleukemia induced by the regressing Friend murine leukemia virus (F-MuLV) complex was inhibited by irradiation of the animals prior to F-MuLV inoculation. This inhibition was proportional to the dose of radiation used. Treatment of the mice with the bone-seeking isotope 89Sr also inhibited erythroleukemia regression, which implicates the same effector mechanisms involved in the resistance to F-MuLV or F-MuLV-induced immunosuprression. Erythroleukemias induced in athymic nude mice by the regressing F-MuLV complex exhibited higher rates of lethality than did the leukemias in heterozygous or homozygous thymus gland-containing controls. These data suggested the involvement of the immune system in erythroleukemia regression and the specific participation of thymus cells and an 89Sr-susceptible function, perhaps marrow-dependent cells, in the process of regression.

Animals↗
PubMed1977

Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component.

The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV-RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV is N-tropic. Passage of nonregressing CFV through Fv-1 incompatible Swiss/ICR mice changed the tropism of CFV from N to NB and resulted in a virus strain which induced erythroleukemia that regressed. Passage of NB-tropic CFV back through Fv-1 compatible mice maintained NB-tropism and regression. Altering the quantity or type of helper MuLV in RFV complex by addition of Ri-MuLV inhibited regression in proportion to the amount of added Ri-MuLV. These studies indicate a relationship between a change in virus tropism to NB by passage in certain hosts (e.g., Swiss/ICR mice) and the ability of Friend virus to induce erythroleukemia that spontaneously regresses. MuLV-RF isolated from the RFV complex induced lymphocytic leukemia in newborn mice which regressed and caused the regression of CFV-induced erythroleukemia. MuLV-RF is NB-tropic, contains no spleen focus-forming virus (SFFV) activity and helps SFFV form spleen foci in genetically restrictive mice. Pseudotype viruses were prepared, consisting of MuLV-RF, or other MuLV's, and SFFV derived from FV-B. The pseudotype viruses each acquired the tropism of the MuLV used in rescue. The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed. These studies demonstrate that the ability of RFV to induce erythroleukemia that spontaneously regresses is due to its helper MuLV component.

Animals↗
PubMed1977

Spontaneous regression of Friend virus-induced erythroleukemia. II. regression of Friend murine leukemia virus-induced lymphocytic leukemia.

We characterized several aspects of spontaneous regression of lymphocytic leukemia in mice. The disease, induced by the helper murine leukemia virus (MuLV) component obtained from the regressing Friend virus complex (RFV), was characterized by spleen and lymph node enlargement, thymus involvement, and anemia. Leukemia regression occurred in about 25% of infected mice and resulted in the return of lymphoid organs to near-normal weight and normal histology and the recovery from anemia. A tenfold to 1,000-fold decrease in virus titer was seen in those mice in which leukemia regressed when compared to leukemic animals, although infectious virus was still recoverable from apparently normal spleens. The sera of mice in which leukemia regressed contained potent virus-neutralizing activity that was associated mainly with immunoglobulins. These studies firmly supported the evidence that the regressing phenotype of RFV was due to its helper MuLV component (MuLV-RF).

Animals↗
PubMed1976

Effects of thymectomy and antithymocyte serum on spontaneous regression of Friend virus-induced erythroleukemia.

To evaluate the role of immune response in regression of leukemia, we studied the effect of immunosuppression on the spontaneous regression of a leukemia induced by a specific strain of Friend murine leukemia virus complex (RFV). Thymectomy of newborn but not adult outbred Swiss mice markedly inhibited regression. The effect of antithymocyte serum (ATS) on regression depended on the timing of ATS treatment. Regression was markedly inhibited in leukemic mice given ATS just before the start of regression. During leukemia development, ATS treatment but not thymectomy potentiated splenomegaly and delayed the start of regression. Both ATS treatment and neonatal thymectomy increased mortality as a function of the decrease in disease regression. Treatment with normal rabbit serum also inhibited regression but, when given during leukemia development, affected neither the splenomegalic response to RFV nor the number of deaths. The data demonstrated that an intact immune system was required for leukemia regression and suggested that some thymus-dependent parameter of immune response was a major factor in regression.

Animals↗
PubMedDate not supplied

Application of an end-systolic pressure-segment length relationship for measuring regional contractility.

A method for estimating regional contractility is described using the end-systolic relationship between left ventricular pressure and myocardial segment-lengths in rapidly volume-loaded beats. The approach was based on the success of previously developed end-systolic relationships between left ventricular pressure and volume and between variable ejection force and fiber length used to describe global contractility in beating hearts. The regional end-systolic relationship was more complicated than its global counterpart, which was load independent, and appeared curvilinear to rapid volume loading. As an approximation of this relationship, a linear slope was constructed between maximum and minimum (pre-ejection) loaded beats of equal cycle length. Because of its load dependency and in order to compare slope relationships between interventions, slope functions were derived only from similarly loaded beats either within or between interventions. Slopes generated by this technique had a reasonable constancy at control conditions and coronary flows with an average SEM of 9.1% of the slope means. End-systolic slopes also appeared sensitive to changes in contractile state, increasing appropriately following treatments with dobutamine and decreasing after propranolol. Following shifts in the end-systolic slopes were unreliable, however, in describing the regional changes in contractility with ischemia. At milder levels of flow restriction, the slopes declined as expected. At moderate levels of flow restriction, the pressure-segment loops shifted markedly rightward and the slope increased. At advanced levels of ischemia, the loops were so distorted, that end-systole could not be identified accurately and the loops essentially described the diastolic compliance characteristics of the left ventricle. Thus the slope estimates of regional contractility as described in this report provided a reliable assessment of inotropic background during modifications with positive and negative inotropic drugs but became invalid as systolic shortening was replaced by aneurysmal bulging during high-grade ischemia.

Animals↗
PubMedDate not supplied

The influence of the route of administration on the bioavailability of an endogenous macromolecule: chondroitin sulphate (CSA).

The absorption of chondroitin sulphate (CSA) has been investigated in rabbits after the oral administration of a single dose of 100 mg of CSA per kg of body weight. The oral dose was administered as a lipid suspension or in enteric capsules. No absorption of CSA could be demonstrated. Oral administration did not cause the release of a clearing factor into the bloodstream, a phenomenon that is known to occur in the presence of CSA. The concentration of this factor did not decrease after oral administration of CSA.

Administration, Oral↗