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Inherited anophthalmia was observed in the progeny of a female rat irradiated with 50 R of X-irradiation at 17 days of age. Observations on the inheritance of the condition indicated that this anophthalmia can be considered as the result of polygenic factors with incomplete penetrance.
Late radiation enteritis is a sequela of radiation therapy to the abdomen. The pathogenic process is poorly understood at the molecular level. cDNA array analysis was used to provide new insights into the pathogenesis of this disorder. Gene profiles of six samples of fibrotic bowel tissue from patients with radiation enteritis and six healthy bowel tissue samples from patients without radiation enteritis were compared using membrane-based arrays containing 1314 cDNAs. Results were confirmed with real-time RT-PCR and Western blot analysis. Array analysis identified many differentially expressed genes involved in fibrosis, stress response, inflammation, cell adhesion, intracellular and nuclear signaling, and metabolic pathways. Increased expression of genes coding for proteins involved in the composition and remodeling of the extracellular matrix, along with altered expression of genes involved in cell- to-cell and cell-to-matrix interactions, were observed mainly in radiation enteritis samples. Stress, inflammatory responses, and antioxidant metabolism were altered in radiation enteritis as were genes coding for recruitment of lymphocytes and macrophages. The Rho/HSP27 (HSPB1)/zyxin pathway, involved in tissue contraction and myofibroblast transdifferentiation, was also altered in radiation enteritis, suggesting that this pathway could be related to the fibrogenic process. Our results provide a global and integrated view of the alteration of gene expression associated with radiation enteritis. They suggest that radiation enteritis is a dynamic process involving constant remodeling of each structural component of the intestinal tissue, i.e. the mucosa, the mesenchyme, and blood vessels. Functional studies will be necessary to validate the present results.
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Osteosarcoma is the most common bone tumor of children and adolescents. The peak incidence of the disease is in the 15 to 19 year age group. The disease is more commonly seen in males than females. While several factors, including exposure to radiation, genetic disorders such as retinoblastoma, and high rate of bone growth, have been associated with osteosarcoma, in most cases no definite etiology can be established. Osteosarcoma usually originates in the metaphyseal region of long bones and extends through the cortex, causing varying degrees of bone destruction and expansion of periosteum. The radiographic appearance caused by this process is often referred to as "sun burst" sign. Positive diagnosis of osteosarcoma is made by histopathology. The histopathological classification of osteosarcoma can also predict the degree of aggressive behavior of this tumor and thus has prognostic significance. Surgery, including amputation or limb-salvage procedure, is the mainstay of treatment of osteosarcoma. It is now unequivocally established that adjuvant chemotherapy will prolong the survival of patients with this disease. Chemotherapy agents often used include platinum derivates, methotrexate, vincristine, cyclophosphamide, adriamycin, actinomycin D, bleomycin and DTIC. Depending on surgical decision, these agents can be used prior to or after the operation. Immediate fitting with prosthesis and provision of appropriate medical and psychological support in the care of these patients is essential.
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The thesis that medical radiation exposures to the general population in the United States are excessive and that urgent steps need to be taken to reduce them is examined. At the present time, no evidence is found that deleterious effects result from radiation exposures at the level of a few rads or less. Nevertheless it is prudent that we assume the possibility of harmful effects of radiation exposure. However, because medical radiology is clearly so beneficial, and the harmful effects are problematical, it is doubtful whether the public should be alarmed by the suggestion of any crisis. A balancing of risks and benefits in the medical uses of radiology supports this latter contention.
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During all the history of the development of radiation biology a problem of "energy paradox"--low consumption of energy of ionizing and non-ionizing radiation in realization of irradiation effect--has been in the focus. The first principle, which contributed much to quantitative concepts of radiation biology, is a hit principle. The hit principle, as is well known, is based on physical properties of ionizing radiations: their discontinuity, quantization and probabilistic distribution in space. Hits, i.e. acts of energy interaction with substance elements, do not depend on each other and are obeyed to Poisson distribution. The other well-known principle--a target principle--is based on the understanding that a living system has some peculiarities: a structure of elements as well as their functions are heterogeneous, unequal and differ in response to the same hits. Along with a unique DNA macromolecule, a critical target structure, biological membranes (BM) with their barrier-matrix, energy and regulatory functions, which make a basis of living processes, are also can be considered as a sensitive target structure. One more principle--a principle of amplification of primary radiation lesions in critical target structures is based on the radiation post-effect, a well-known phenomenon in radiation biology. The fourth principle is a principle of target damage recovery (regulations of cell homeostasis) that means a system response to irradiation involving mechanisms of protection and reparation of lesions in DNA and BM. The progress in molecular biology and radiation biophysics achieved for the last two decades provided an especially powerful impetus to the development of those principles, which are based on the analysis of the radio-biological effects developing in time. The main principles of radiation biology consider peculiarities of physical and biological action of ionizing radiation.
According to the analysis of epidemiological and experimental data there are evidences in threshold on criterion of mutagenic (in broad sense) ionising radiation action. A threshold takes place in the region of about 20-200 mGy concerning a dose in case of an acute exposure and in the region of the third order above a background level regarding a dose rate in case of chronic or prolonged exposure. Evidences in favour of linear non-threshold conception are based on primitive mathematical extrapolations and approximations of the study results, mainly, in the region of intermediate doses/dose rates. Besides real data in region of low doses are ignored. The latter has a reason in paradigm of stochastic damage action of ionising radiation and in underestimation of cell and organism protection-reparation systems action. Regarding axiomatic bases of ionising radiation action it is possible to conclude more reliable substantiation of the dual (positive-negative) nature and the threshold conception concerning ionising radiation action in comparison with the non-threshold one.