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Biomedical subjects

R Myers

Publications and source records attributed to R Myers.

At least 145 records · Page 8Linked to original sources
PubMed1984

An unexpected effect of hyperthermia on the expression of X-ray damage in mouse skin.

The interaction between hyperthermia and X irradiation in the expression of injury to skin was investigated in the tail of adult mice. The X-ray treatments when given alone resulted in skin reactions which ranged in severity from "no observable gross injury" to "moist desquamation over most of the tail," the peak reaction occurring at approximately 20 days. When hyperthermia was given alone, the maximal reaction observed was "foci of moist desquamation, accompanied by severe erythema and edema" which, in contrast to the radiation response, peaked 1 to 2 days after treatment. For the combined treatments, hyperthermia at a temperature between 43.0 and 44.5 degrees C for 30 min was given either 3, 6, 9, or 10 days after X irradiation. When the interval was 3 days, there appeared to be no interaction between the treatments. As the interval was lengthened, so that hyperthermia was given 6 or more days after irradiation, i.e., within 7 days of the time of appearance of gross radiation injury, the severity of the observed skin reaction was greater than the individual responses following either treatment given alone. Using a 9-day interval, it could be seen that both the thermal and radiation reactions were enhanced in a dose-dependent manner. The peak times for each reaction were not significantly altered by the additional treatment. The results are discussed with reference to possible modes of interaction between X irradiation and hyperthermia in an in vivo system.

Animals↗
PubMed1983

Photoaffinity labeling of the indole sites on the Escherichia coli tryptophan synthase alpha-subunit.

The alpha subunit of the Escherichia coli tryptophan synthase catalyzes the reversible aldolytic reaction: Indole-3-glycerol phosphate in equilibrium indole + glyceraldehyde 3-phosphate. The use of 5-azidoindole as a photoaffinity label has made the generation of a number of enzyme-substrate complexes possible, each with a given degree of saturation of the two postulated indole sites. When assayed in the reverse reaction (indole-3-glycerol phosphate synthesis), samples of alpha subunit treated at concentrations of 5-azidoindole less than or equal to 2 mM show a progressive 30-40% activation. A gradual inactivation occurs only in samples irradiated at concentrations in excess of 2 mM 5-azidoindole, and this inactivation is complete at 8-10 mM. A quantitatively similar activation occurs in the forward reaction (indole synthesis), however inactivation in this case is incomplete, with complexes treated at 8-12 mM 5-azidoindole retaining 30-40% relative activity in this reaction. When treated alpha subunits were assayed for their abilities to complement the beta 2-subunit in the reactions indole + L-serine leads to L-tryptophan + H2O and indole-3-glycerol phosphate + L-serine leads to L-tryptophan + glyceraldehyde 3-phosphate, quantitatively lesser amounts of activation followed by total inactivation are observed over a similar range of 5-azidoindole concentrations.

Affinity Labels↗
PubMed1983

An unusual autoimmune hemolytic anemia in a patient with immunoblastic sarcoma.

This report describes a patient with immunoblastic sarcoma and autoimmune hemolytic anemia with reticulocytopenia and red cell hypoplasia. Both IgG and IgM red cell autoantibodies were present in the patient's serum, and both antibodies had the uncommon specificity of anti-IT. This report appears to be the first to describe IgG auto anti-IT and autoimmune hemolytic anemia in a patient who did not have Hodgkin's disease; the laboratory findings and clinical course are described. The reticulocytopenia and red cell hypoplasia may have been immunologically mediated. The patient responded to plasma exchange, corticosteroids, and chemotherapy.

Anemia, Hemolytic, Autoimmune↗
PubMed1983

Nerve compression injury and increased endoneurial fluid pressure: a "miniature compartment syndrome".

An inflatable miniature cuff was used to apply local compression of 80 mm Hg or 30 mm Hg to a segment of rat sciatic nerve for time periods varying from two to eight hours. The endoneurial fluid pressure was measured by direct micropipette measurement techniques at one or 24 hours after removal of the cuff, and the nerves were subjected to histological analysis. Endoneurial oedema, associated with a four-fold increase in endoneurial fluid pressure, was observed after compression at 80 mm Hg for four hours, and a three-fold increase was found after compression at 30 or 80 mm Hg for eight hours. Such an increase in endoneurial fluid pressure may interfere with intrafascicular capillary flow, and thereby constitute an important pathophysiological mechanism in nerve compression injuries.

Animals↗
PubMed1982

A comparison of thermal enhancement ratios for fast neutron and x irradiation of two normal tissues in rodents.

The effects of a hyperthermal treatment of one hour on radiation damage to baby rat cartilage and mouse intestine were compared for 250 kVp X irradiation and cyclotron-produced neutron irradiation (mean energy of about 7.5 MeV). Heat, in the range 41.0 degrees C-43.0 degrees C, caused no observable gross tissue injury when given alone. When heat was given immediately before radiation, the radiation damage was enhanced. There was no qualitative differences between response after fast neutrons and after X rays. Thermal enhancement ratios (TER) were similar for the two tissues and were not affected by the type of radiation used. Thus, the relative biological effectiveness (RBE) of fast neutrons compared with X rays was not markedly altered by combining radiation with hyperthermia.

Animals↗
PubMed1982

Histology of the irradiated rat brain in the first post-irradiation year.

The histology of the brains of rats killed were studied, following various doses of 250 kV X rays. The majority of rats which were killed before 200 days showed no damage to the mid-brain and cerebral hemispheres. However, the trigeminal and facial nerves exhibited necrosis, the origin of which was probably in the central nervous tissue of the transitional region between central and peripheral nerve systems. The result of these lesions was atrophy of the masticatory muscles and a consequent difficulty in feeding. Rats surviving beyond 200 days post-irradiation exhibited focal necrosis within central white matter regions which resembled, both in form and location, those described in previous reports for rats.

Animals↗
PubMed1982

Residual injury in the spinal cord after treatment with X rays or neutrons.

Residual injury in the spinal cord 100 days after X rays or neutrons was measured by the reduction in dose of a second radiation required to produce nerve damage assessed by the development of ataxia within the first post-irradiation year. Between 5-10% residual damage was observed after X-ray doses of 25% or 50% of the single X-ray dose which produced ataxia in 50% of animals (ED50), but 30% residual injury was observed if the X-ray dose was 75% of the ED50 dose. Neutron doses of 25% and 50% of the ED50 neutron dose gave the same level of residual injury as observed after equivalent X-ray doses, indicating that for this type of damage the shedding of residual damage was similar after X rays or neutrons. More residual damage is observed after a dose of X rays for vascular related damage than for damage associated with glial cell loss. However, if residual damage is expressed in terms of the relevant vascular or glial cell damage caused by the priming dose the same relationship between primary damage and residual damage is seen for both glial and vascular related damage.

Animals↗
PubMed1981

Turnover of proliferative cells in the spinal cord after X irradiation and its relation to time-dependent repair of radiation damage.

The changes in labelling index of neuroglial cells of the rat cervical cord following 20 Gy X rays are compared with the timing and pattern of the repair of radiation damage in the spinal cord. The start of time-dependent repair coincides with the release of the proliferative neuroglia from a block at the G1/S border. The evidence suggests that the time-dependent repair reflects the normal unstimulated proliferation of the surviving neuroglial cells and that homeostatically stimulated recruitment to the proliferative neuroglia does not occur until the period just before the development of paralysis. A normal cell-cycle time of about one month for the spinal cord neuroglia is indicated from the observed pattern of labelling.

Animals↗
PubMed1980

Regulation of simian virus 40 early transcription in vitro by a purified tumor antigen.

Cloned DNA templates were used to direct the transcription of early and late simian virus 40 (SV40) genes by a cell-free RNA-synthesizing system. Transcription by RNA polymerase II was sensitive to low levels of alpha-amanitin and completely dependent on exogenously added DNA template. RNA products of discrete lengths were efficiently synthesized when transcription was directed by DNA restriction fragments containing promoter sequences for either early or late genes of SV40. Addition of the D2 tumor antigen to the template DNA inhibited transcription originating from the SV40 early promoter. In contrast, the D2 protein had little or no effect on the transcription from SV40 or adenovirus 2 (Ad2) late promoter sequences. When a mixture of cloned DNA containing SV40 early promoter and Ad2 late promoter was used to direct RNA synthesis, the D2 protein specifically inhibited the synthesis of SV40 early genes but not that of Ad2 late sequences. The D2 DNA binding protein also had no effect on the transcription directed by SV40 mutant templates that contain an intact early promoter sequence but lack specific tumor-antigen binding sites. We have confirmed that, under the conditions of the transcription assay, the D2 protein binds and interacts specifically with its recognition sites on wild-type template DNAs but fails to bind to mutant or Ad2 DNA templates that lack sequences containing SV40 tumor-antigen binding sites. These findings provide evidence that a direct interaction between tumor antigen and its specific binding sites on DNA is the mechanism by which the SV40 A gene autoregulates its transcription.

Antigens, Neoplasm↗
PubMed1980

The relationship between heating time and temperature for inhibition of growth in baby rat cartilage by combined hyperthermia and X-rays.

The relationship between the Thermal Enhancement Ratio (TER) for X-ray damage and time of heating has been investigated in epiphyseal rat cartilage. The TER at each temperature rises steeply with increasing heating time. Data obtained using various heat treatments with 8 Gy of X-rays have been analysed in terms of stunting "rate' as measured by the slope of the dose-effect curve obtained for each temperature. The "rate' of stunting per unit heating time, induced by thermally enhanced X-ray damage is compared with the "rate' of stunting induced by heat alone. The two are similar each having an activation energy of approximately 550kJ mole-1, as determined using the Arrhenius equation. Halving the heating time requires at 1 degrees C temperature increase to achieve the same degree of thermal enhancement of X-ray damage. Similar results have been reported previously for damage caused by heat alone. Over a range 42 degrees C-45 degrees C, the threshold heating time to cause direct thermal injury falls within the range of times used to enhance X-ray damage. It is suggested that a component of damage due to direct thermal injury, indistinguishable from radiation damage and thermally enhanced radiation damage, will contribute to TER assessments in some experimental systems.

Animals↗
PubMed1979

The relationship between o.e.r., r.b.e. and number of fractions for X-ray- or neutron-induced skin damage.

The skin reactions in aerated and hypoxic mouse tails after single or fractionated doses of 250 kV X-rays or fast neutrons (6 MeV deuterons on beryllium) have been measured. The o.e.r. for one to sixteen fractions of X-rays remains constant, while that for one to ten fractions of neutrons decreases with increasing neutron fractionation and decreasing neutron dose/fraction. The o.e.r. for X-rays was 1.7, for single-neutron doses 1.4, and for ten fractions of neutrons 1.25. It was anticipated that the o.e.r. for neutron-induced damage would decrease further as neutron fractionation is increased because the contribution to damage from the highest LET components of dose, the alpha and heavy recoil particles, would increase relative to the lowe LET components. The r.b.e. values obtained for skin damage were higher at all neutron doses/fraction examined in this study on tails than all those previously obtained in studies on skin at other sites on four species. This may be due to the influence of hypoxia on the r.b.e. measurements in the mouse tail.

Animals↗