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At least 19 recordsLinked to original sources
PubMed1991

Radiation effects on the immunological functions and membranes of alveolar macrophages of rats.

Alveolar macrophages (AM) from BCG activated Wistar rat were irradiated with different doses of Gamma rays in vitro. The effects of radiation on their immunological functions and membrane damage were studied. The non-specific cytotoxicity and specific phagocytosis of AM irradiated with dose of 0, 100, 300 and 500 Gy decreased with the increase in dose. The relative fractions of Lactate Dehydrogenase and Beta-glucuronidase (beta-glu) activity in supernatant increased with the increase in dose. There was a correlation between the suppression of immunological functions and the degree of damage of cytoplasmic and lysosomal membranes of AM after irradiation. Na2SeO3, a protective agent of cell membranes, alleviated this effect on the suppressive cytotoxicity indices of irradiated AM.

Animals↗
PubMed1990

Radiation effect of gadolinium-neutron capture reactions on the survival of Chinese hamster cells.

In gadolinium-neutron capture reactions, prompt gamma rays with an energy spectrum of up to 7 MeV, X-rays and electrons are released. We measured the effect of radiation as a result of capture reactions on cultured Chinese hamster cells. Cells in the medium containing 5000 ppm gadolinium were exposed to thermal neutrons from a nuclear reactor. The survival curve for those cells exhibited a shoulder in the low neutron fluence region. The survival curve for cells exposed to thermal neutrons in the absence of gadolinium was a simple exponential function. To obtain 10% survival levels, 5.4 x 10(12) neutrons/cm2 were required for cells irradiated in the absence of gadolinium, and 1.55 x 10(12) neutrons/cm2 for those irradiated in the presence of gadolinium. The therapeutic ratio in gadolinium-neutron capture therapy depends on the difference in 157Gd concentrations between the tumor and normal tissues. Thus, our current effort has been to develop a method of selectively delivering 157Gd to tumors.

Animals↗
PubMed1989

[Radiation effects on expression of FC-receptor of alveolar macrophages of rat and their specific phagocytosis].

BCG-activated alveolar macrophages (AM) of Wistar rats were irradiated with different doses of gamma-ray in vitro. The effects of radiation on the expression of their Fc-receptor and specific phagocytic activity were observed. AM, after irradiation with doses of 0, 100, 300 and 500 Gy, showed decreasing phagocytic activity to chicken red blood cells (CRBC) opsonized with anti-CRBC antibody with no change in phagocytic indices. The expression of Fc-receptor of AM was, however, increased.

Animals↗
PubMed1988

Assay of radiation effects in mouse skin as expressed in wound healing.

The effect of 150 kVp X irradiation on the healing of full depth surgical wounds in the lower dorsal skin of the mouse was assayed by measuring the wound strength of seven 2-mm-wide segments along each wound. The strength of unirradiated wounds increased with time in two phases: during the first 2 weeks it reached nearly half of the values recorded from unwounded skin, after which the rate of increase slowed for at least 2 weeks before beginning a second increase. By 150 days, the breaking strength of the wound was about 80% of that of unwounded skin. A single dose of 18 Gy prior to wounding reduced the strength of the wounds to about one-third to one-half that of an unirradiated wounds within the 3 months of follow-up. The effect of irradiation on wound strength did not change as the interval between exposure and wounding was increased to 2 months but decreased slightly when this interval was extended to 3 months. When the healing wound was irradiated within 5 days of surgery, the effect on healing was about the same as with preirradiation; if irradiation was delayed for 12 days after wounding the second phase of healing was only postponed and the wound strength ultimately approached the values recorded from unirradiated wounds. The wound strength of skin preirradiated by X rays and assayed 14 days after wounding showed a clear sigmoid dose response with a threshold between 8 and 10 Gy and a plateau at the maximum effect above 20 Gy. The persistence for at least 3 months of the effect of radiation on wound healing suggests that the tissues involved in the healing process are normally proliferating slowly. The accelerated expression of radiation injury through surgical wounding permits the early quantification of the radiation response of tissues that would normally be delayed in their expression of radiation damage.

Animals↗
PubMed1977

Chemical modification of radiation effects.

A number of powerful chemical compounds that modify radiation effects have been discovered and tested both in the laboratory and clinically over the past 25 years. There are four major classes of compounds: aminothiol radio-protectors which act on well vascularized euoxic cells and concentrate in tissues such as skin, gut and marrow; nitromidazole radiosensitizers which act on hypoxic tumor cells; pyrimidine analogues which are incorporated into the DNA of cycling cells and cause radiosensitization; and cancer themotherapy agents which, in addition to their ability to kill tumor cells directly, also may sensitize tumor and normal cells to radiation. The mechanism of action, experimental activity, and clinical results or the potential for each of these agents are reviewed.

Animals↗
PubMed1977

Cumulative radiation effect. Part VII: computer calculations and applications in clinical practice.

In five previous papers, the concept of the Cumulative Radiation Effect (CRE) has been presented as a scale of accumulative sub-tolerance radiation damage. The biological effect generated in normal connective tissue by fractionated or continuous radiation therapy given in any temporal arrangement is described by the CRE on a unified scale of assessment, so that a unique value of the CRE describes a specific level of radiation effect. The basic methods of evaluating CREs were shown in the papers to facilitate a full understanding of the fundamental aspects of the CRE-system, but these methods can be time-consuming and tedious for complex situations. In the previous papers in this series, one way of overcoming the difficulties in evaluating CRE problems was presented in simple nomographic and tabular methods for the solution of practical problems. An alternative way of overcoming the difficulties in the evaluation of CRE problems is to use computers and it is the purpose of this paper to outline computer calculations and applications in clinical practice in connection with the CRE-system. In a general appraisal of the applications of computers to the CRE-system, the various problems encountered in clinical radiotherapy are categorised into those involving the evaluation of a CRE at a point in tissue and those involving the calculation of CRE distributions. As a general guide, the computer techniques adopted at the Glasgow Institute of Radiotherapeutics for the solution of CRE problems are presented, and consist basically of a package of three interactive programs for point CRE calculations and a Fortan program which calculates CRE distributions for iso-effect treatment planning. Many examples are given to demonstrate the applications of these programs, and special emphasis has been laid on the problem of treating a point in tissue with different doses per fraction on alternate treatment days. The wide range of possible clinical applications of the CRE-system has been outlined and described under the categories of routine clinical applicatons, retrospective and prospective surveys of patient treatment, and experimental and theoretical research. Some of these applications such as the results of surveys and studies of time optimisation of treatment schedules could have far-reaching consequences and lead to significant improvements in treatment and cure rates with the minimum damage to normal tissue.

Computers↗
PubMed1977

Cumulative radiation effect. Part VI: simple nomographic and tabular methods for the solution of practical problems.

In five previous papers, the concept of the Cumulative Radiation Effect (CRE) has been presented as a scale of accumulative sub-tolerance radiation damage. The biological effect generated in normal connective tissue by fractionated or continuous radiation therapy given in any temporal arrangement is described by the CRE on a unified scale of assessment, so that a unique value of the CRE describes a specific level of radiation effect. The basic methods of evaluating CREs were shown in these papers to facilitate a full understanding of the fundamental aspects of the CRE-system, but these methods can be time-consuming and tediuous for complex situations. In this paper, simple nomographic and tabular methods for the solution of practical problems are presented. An essential feature of solving a CRE problem is firstly to present it in a concise and readily appreciated form, and, to do this, nomenclature is introduced to describe schedules and regimes as compactly as possible. Simple algebraic equations are derived to describe the CRE achieved by multi-schedule regimes. In these equations, the equivalence conditions existing at the junctions between schedules are not explicit and the equations are based on the CREs of the constituent schedules assessed individually without reference to their context in the regime as a whole. This independent evaluations of CREs for each schedule results in a considerable simplification in the calculation of complex problems. The calculations are further simplified by the use of suitable tables and nomograms, so that the mathematics involved is reduced to simple arithmetical operations which require at the most the use of a slide rule but can be done by hand. The order of procedure in the presentation and calculation of CRE problems can be summarised in an evaluation procedure sheet. The resulting simple methods for solving practical problems of any complexity on the CRE-system are demonstrated by a number of examples.

Connective Tissue↗
PubMed1979

Cell survival description of the cumulative radiation effect.

An equation is proposed to link the Cumulative Radiation Effect (CRE) scale of radiation damage with the fraction of basal cells surviving after irradiation of skin epithelium. The model assumes an expression for the basal cell survival curve which fits the various hit-target models over the range of doses found in clinical practice. The model is consistent with CRE in the dependence on total treatment dose and fractionation number. A 'first order' analysis using a Gompertzian re-growth of cells also yields reasonable agreement with the CRE equation in time dependence during treatment and during a gap. This model is suitable for acute skin reactions but not necessarily for late effects in connective tissue.

Cell Survival↗
PubMed1986

Predictive biochemical assays for late radiation effects.

Surfactant precursors or other products of Type II pneumocytes have the potential to be the first biochemical marker for late radiation effects. This is particularly clinically important in the combined modality era because of the frequent occurrence of pneumonitis and pulmonary fibrosis secondary to radiation or chemotherapy. Accordingly, correlative studies have been pursued with the Type II pneumocyte as a beginning point to understand the complex pathophysiology of radiation pneumonitis and fibrosis. From our ultrastructural and biochemical studies, it is evident that Type II pneumocytes are an early target of radiation and the release of surfactant into the alveolus shortly after exposure persists for days and weeks. Through the use of lavaging techniques, alveolar surfactant has been elevated after pulmonary irradiation. In three murine strains and in the rabbit, there is a strong correlation with surfactant release at 7 and/or 28 days in vivo with later lethality in months. In vitro studies using cultures of type II pneumocytes also demonstrate dose response and tolerance factors that are comparable to the in vivo small and large animal diagnostic models. New markers are being developed to serve as a predictive index for later lethal pneumonopathies. With the development of these techniques, the search for early biochemical markers in man have been undertaken. Through the use of biochemical, histological, and ultrastructural techniques, a causal relationship between radiation effects on type II pneumocytes, pulmonary cells, endothelial cells of blood vessels, and their roles in the production of pneumonitis and fibrosis will evolve.

Animals↗
PubMed1975

Skin reactions after different fractionation schedules giving the same cumulative radiation effect.

The CRE formula was used for calculation of biologically equivalent radiation doses with different fractionation schedules. The early radiation effects, skin erythema and pigmentation were measured with a reflectance spectrophotometer at wavelengths 578 and 660 nm. The course and maximum for both erythema and pigmentation agreed well with the two types of fractionation. The results seem to justify further use of this simple formula.

Breast Neoplasms↗
PubMed1978

Radiation effects on the fine blood vessels in abdominal organs of mice.

The capillary networks of normal and irradiated abdominal organs of mouse were investigated by a resin cast technique. The structure of the capillary system had characteristic appearances. Radiation effects on the fine vascular structures were demonstrated from one appearances. Radiation effects on the fine vascular structures were demonstrated from one to 30 days after a single dose of 5 to 30 Gy whole body irradiation. Prominent morphologic abnormalities of the shape and distribution of the capillaries were identified, especially in the small intestine.

Abdomen↗
PubMed1989

[Dose, radiation effect and initial symptoms following unexpected whole body irradiation: an analysis of 19 accidents].

The radiation induced effects on the haemopoietic system and the human body after acute unexpected whole body irradiation are manifold. Therefore it is meaningful to incorporate the scientific foundations of radiation effects in the available knowledge about the consequences of radiation exposure. From this aspect the present paper evaluates 19 acute radiation accidents which were published between 1945 and 1986 in the scientific literature involving about 597 individuals. Even in the case of an uncomplicated radiation effect the physician must not rely on the estimated physical dose because it does not or does not necessarily correlate with the different course of events taken by the individual categories of the acute radiation syndrome. In fact, the dose is of minor importance to the physician because as a rule it can only be determined too late due to the complex parameters. The classification, therapy and prognosis of the accident victims is largely governed by the pathophysiology which results from the random probability of the cell killing mechanisms by radiation, inhomogeneous dose distribution and the scattered distribution of the haemopoietic system in the human body. The fact that in the case of accidentally induced total body irradiation there is only inhomogeneous distribution of radiation dose is a life-saving factor in most cases. Furthermore, it is pointed out that by means of simple diagnostic methods, e.g. the initial symptoms, the first classification of accident victims is also largely possible without referring to the dose.

Accidents↗
PubMed1990

Cancer risk among children of atomic bomb survivors. A review of RERF epidemiologic studies. Radiation Effects Research Foundation.

This article summarizes recent epidemiologic studies of cancer risk among the children of atomic bomb survivors conducted at the Radiation Effects Research Foundation. These children include two groups: (1) the in utero-exposed children (ie, those born to mothers who had been pregnant at the time of the bombings of Hiroshima and Nagasaki) and (2) the F1 population, which was conceived after the atomic-bombings and born to parents of whom one or both were atomic bomb survivors. Although from 1950 to 1984 only 18 cancer cases were identified among the in utero sample, cancer risk did appear to significantly increase as maternal uterine dose increased. However, since the observed cases are too few in number to allow a site-specific review, the increased cancer risk cannot be definitively attributed to atomic bomb radiation, as yet. For those members of the F1 population who were less than 20 years old between 1946 and 1982, cancer risk did not appear to increase significantly as parental gonadal dose increased. Follow-up of this population will continue to determine if the patterns of adult-onset cancer are altered.

Abnormalities, Radiation-Induced↗