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Biomedical subjects

R A Steeves

Publications and source records attributed to R A Steeves.

At least 55 records · Page 3Linked to original sources
PubMed1982

A comparison of various types of patient instruction in the proper administration of metered inhalers.

The administration technique employed by 42 inpatients using metered inhalers were observed. Proper performance of the six steps recommended by the manufacturer provided the guidelines for correct administration. The degree of compliance with proper technique was defined as the number of steps correctly executed by the patient. The mean number of steps correctly performed was 2.9 out of the possible six (48.3 percent). Twenty-four patients were then randomized into one of three groups. Group I received the manufacturer's instruction sheet, Group 2 received counseling from a pharmacist, and Group 3 received both the manufacturer's instruction sheet and counseling from a pharmacist. There was a significant improvement in the postinstruction technique in Groups 2 and 3, while Groups 1 failed to demonstrate any significant improvement. Comparisons were then made among the three groups. No significant difference was found between Group 2 and Group 3. However, both Groups 2 and 3 were found to be significantly different (p less than 0.05) from Group 1. This study shows that pharmacist counseling can significantly improve the degree of patient compliance in the administration of metered inhalers.

Aerosols↗
PubMed1981

Neoplasms induced by megavoltage radiation in the head and neck region.

Radiation-induced cancer, although fortunately a rare complication of radiotherapy, is nonetheless observed occasionally even after megavoltage radiation has been used. Over a 22-year period at the Curie Institute, four patients were found to have malignant neoplasms within the fields of megavoltage treatment given for various cancers of the head and neck region. Three of the neoplasms were sarcomas, two osteogenic and one fibrosarcoma, and the other tumor was a sarcomatoid epithelioma. The latent period ranged from 3 1/2-15 years. Although the evidence is strong that the neoplasms were causally related to the precedent irradiation, it is acknowledged that rare examples of the "double primary" phenomenon exist, even separated by five or more years, and that only one such instance would induce a large error in the estimated frequency of postirradiation neoplasms. Because clinical estimates after megavoltage irradiation are usually compounded by an association with a relatively high total absorbed dose, the issue of the incidence of postirradiation neoplasms as a function of the type of external beam (orthovoltage vs. megavoltage) may require resolution by experimental means. Another rare sequela of radiotherapy is injury to a peripheral nerve. One of the four patients with a second neoplasm after radiation also developed left hypoglossal nerve palsy 2 1/2 years post-therapy, and left optic nerve atrophy seven years postradiation treatment of a squamous cell carcinoma of the ethmoid and maxillary sinuses. The 51-year-old patient had received a tumor dose of 6800 rads (2043 rets).

Carcinoma, Squamous Cell↗
PubMed1981

Spleen focus-forming virus: specific neutralization by antisera to certain gag gene-encoded proteins.

Immunization of rats with syngeneic cells infected with spleen focus-forming virus (SFFV) but not with its helper, Friend murine leukemia virus (FMuLV), produces antisera which specifically neutralize SFFV, and not FMuLV, in the Friend virus complex. To determine which SFFV-encoded protein molecule bears the antigen recognized by these neutralizing antibodies, we studied different lots of rat anti-SFFV antiserum by immunoprecipitation and virus neutralization assays. The ability of these sera to neutralize SFFV correlated with the titer of antibodies to p45gag and not with the titer of those to gp52, suggesting that the neutralizing antibodies recognize the p45gag molecule. To verify this specificity for p45gag, we tested antisera to various MuLV gag gene-encoded proteins for neutralization of SFFV. Goat anti-Rauscher murine leukemia virus (RMuLV) p30 and goat anti-RMuLV p10 sera neither precipitated p45gag from SFFV-infected nonproducer cells nor neutralized SFFV. In contrast, goat anti-RMuLV Pr65gag and goat anti-RMuLV p12 sera precipitated p45gag from SFFV-infected cells and also specifically neutralized SFFV in the Friend virus complex. These findings suggest that, unlike the gag proteins coded for by FMuLV, the proteins coded for by defective SFFV are incorporated into the envelope of virions carrying the SFFV genome, but not into the envelope of those carrying the helper FMuLV genome.

Animals↗
PubMed1979

Specific neutralization of defective spleen focus-forming virus in Friend virus complex by rat antiserum.

The spleen focus-forming virus (SFFV), a rapidly transforming, replication-defective virus in Friend virus (FV) complex that is readily neutralized by antisera directed against its helper virus, was examined for the presence of SFFV-specific antigens. Antisera prepared in Fisher rats against an SFFV-infected Fisher rat embryo fibroblast line (SFFV-FRE) neutralized SFFV effectively, but not Friend-associated murine leukemia virus (F-MuLV) whether the latter was tested alone or was mixed with SFFV in the FV complex. In contrast, serum from mice immunized with SFFV-infected nonproducer mouse cells had little or no neutralizing activity against SFFV. Both absorption and immunoprecipitation studies indicate that the SFFV-specific antigen is immunologically related to xenotropic murine leukemia virus antigens. The role of both SFFV- and F-MuLV-specific antigens in the neutralization of SFFV suggests that this defective virus could be an antigenic mosaic and that viruses in the FV complex may participate in a undirectional form of phenotypic mixing.

Animals↗
PubMed1976

Bacterial lipopolysaccharides as helper factors for Friend spleen focus-forming virus in mice.

Lipopolysaccharide (LPS) from several gram-negative bacteria significantly increased the spleen focus-forming efficiency of N-topic Friend virus complex in mice by different mechanisms. One effect was associated with an increase in the number of availability of potential target cells for spleen focus-forming virus (SFFV) in fully susceptible mouse strains. This enhancing effect was optimal when LPS was injected 5 days before SFFV but was nil when LPS and SFFV were given at the same time. In contrast, in mice genetically resistant to the native helper virus of SFFV, the helper effect of LPS was optical when it was injected with SFFV and oil when given 5 days before or after the virus. LPS did not affect helper virus expression in a standard cell culture (XC) assay, but it did increase helper virus replication in mice. Mice lacking T cells or complete endogenous murine leukemia virus genomes were just as sensitive to the helper effects of LPS on SFFV expression as were control animals. Most of the helper activity of LPS is associated with the lipid A component. The mechanism of the helper effect of lipid A is still unknown, but hypotheses must take into account that this effect did not occur in fully susceptible hosts, but only in hosts carrying resistance alleles at either the FV-1 or the FV-2 locus.

Animals↗
PubMed1976

The Fv-2r resistance gene in mice: its effect on spleen colony formation by Friend virus-transformed cells.

To determine the mechanism by which the recessive Fv-2r gene confers complete resistance to spleen focus formation and to the induction of early splenomegaly characteristic of the Friend virus (FV) disease syndrome, we compared the parameters of FV infection in susceptible DBA/2 (D2) (Fv-1n, Fv-2s) and partially congenic D2.Fv-2r (Fv-1n, Fv-2r) mice. After infecting these mice with N-tropic FV complex, we followed the replication of spleen focus-forming virus (SFFV) and the generation of SFFV-transformed tumor colony-forming cells (CFC) in their spleens. By both parameters D2.Fv-2r mice were 20- to 100-fold less susceptible than DBA/2 controls, but the inhibition was only partial. Transplantation of washed spleen cells from SFFV-infected DBA/2 mice resulted in equal growth and recovery of tumor CFC from both D2.Fv-2r and Fv-2s mice. However, these tumor cells grew as colonies in Fv-2s mice, whereas they grew diffusely in the spleens of D2.Fv-2r hosts and did not develop into macroscopically or microscopically visible colonies. Thus the completeness of the resistance to spleen focus formation that defines the Fv-2r gene was reflected only in the complete suppression of the colonial growth of tumor cells, whereas the other parameters of infection showed no or only partial inhibition.

Animals↗
PubMed1975

Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice.

BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we investigated the expression of FV-associated cell surface antigens on cultured, FV-trnasformed cell lines of BALB.B and BALB/c origin. Both cell lines induced transplantation immunity in syngeneic hosts toward further implantations of the same tumor, BALB.B cells being significantly more potent in this respect than BALB/c cells. BALB.B tumor cells, which produce complete, infectious FV, expressed both the cell surface antigen, FMR (corresponding to the cytotoxic antibodies in anti-FV antisera), and virus envelope antigen (VEA, corresponding to the virus-neutralizing antibodies in the anti-FV antisera). BALB/c tumor cells, on the other hand, which are FV-nonproducers, expressed no FMR antigen, but did express VEA on their surfaces for at least 100 passages in culture. These cells could induce FV-neutralizing but not cytotoxic anti-FMR antibodies when used to immunize syngeneic hosts. The absence of FMR antigen may be the basis for the reduced capacity of BALB/c tumor cells, by comparison with BALB.B tumor cells, to induce transplantation immunity. After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts. This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line.

Animals↗
PubMed1975

Nonviral helper factors for leukemia virus expression in mice.

Nonviral helper factors as well as murine leukemia viruses (MuLV) can increase the infectivity of Friend spleen focus-forming virus (SFFV) in mice which restrict its natural helper virus. Such factors have been isolated from cell-free extracts of human leukemic spleens, bacteria, and mycoplasmata. Unlike immunodepressants and target cell stimulators (which can also increase the pathogenicity of SFFV if applied before infection), nonviral helper factors are most efficient when they are injected with SFFV into helper virus-restrictive mice. In these respects the nonviral factors resemble MuLV. However, helper factors differ from MuLV by their inability to replicate in neonatal mice and by their greater stability to heat. Although the human leukemic helper (HuLV) extracts examined lack detectable mycoplasma or bacterial contamination, the helper assay in mice will be of limited value as a possible detection system for human leukemogenic viruses until a unique marker is found by which to distinguish HuLH activity from that of prokaryotic origin. This makes a systematic comparison among the nonviral helper factors all the more important.

Animals↗
PubMed1974

Structural proteins of mammalian oncogenic RNA viruses: murine leukemia virus neutralization by antisera prepared against purified envelope glycoprotein.

Goat and rabbit antisera prepared against a purified Rauscher murine leukemia virus glycoprotein (gp69/71) rapidly neutralized spleen focus-forming virus in Rauscher and Friend virus preparations. Absorption studies revealed that most of the neutralizing activity of goat anti-Rauscher virus gp69/71 serum was directed against type- and group-specific determinants.

AKR murine leukemia virus↗
PubMed1972

A classification of the murine leukemia viruses. Neutralization of pseudotypes of Friend spleen focus-forming virus by type-specific murine antisera.

Coinfection of neonatal BALB/c mice with helper-dependent Friend spleen focus-forming virus (SFFV), as contained in the Friend virus (FV) complex, and antigenically distinct Moloney leukemia virus (MolLV) resulted in the recovery of a MolLV pseudotype of SFFV, abbreviated SFFV(MolLV). The antigenic alteration of SFFV was observed by following its neutralization kinetics in vitro by specific Friend or Moloney typing antiserum. Effective pseudotype production was accomplished only when N-tropic LLV-F (the natural helper virus in the FV complex) was inhibited in B-type mice coinfected with an NB-tropic MolLV or other murine leukemia virus (MuLV) preparation. SFFV pseudotypes could not be prepared by using murine viruses other than leukemia viruses. SFFV prepared after two serial passages in the presence of MolLV was effectively neutralized by Moloney antiserum, but not by Friend typing antiserum; therefore, the envelope of the pseudotype virus, SFFV(MolLV), is homogeneous. Pseudotype virus was antigenically stable in the absence of continued mixed infection of BALB/c mice with SFFV(MolLV) and MolLV. However, SFFV(MolLV) was easily converted back to the LLV-F type after only one passage in BALB/c mice coinfected with NB-tropic LLV-F. The antigenic interconversion between LLV-F and MolLV types demonstrated that SFFV is defective with respect to the expression of neutralizable envelope antigens. Analysis of the neutralizable envelope antigens of nine SFFV(MuLV) pseudotypes by a panel of seven typing antisera made possible a "type-specific" SFFV(MuLV) envelope classification. Two major categories have been identified which correspond to the Gross (G) and Friend-Moloney-Rauscher (FMR) subgroups. Further, the FMR subgroup was divided into four types on the basis of distinct neutralization patterns. These results indicated that the specificity observed by cytotoxic G vs. FMR antisera is different from that observed by neutralization kinetics. We therefore suggest that the specific antigens revealed by virus neutralization tests be referred to as type specific.

Animals↗