カテゴリー「neurology」
Author: M. Yang, J.S. Kim, M.S. Song et al.
Reference: Int. J. Radiat. Biol. ― 2010. ― Vol. 86, № 6. ― P. 476–485.
Keywords: linear energy transfer, hippocampal dentate gyrus, mice
Abstract: PURPOSE: Our study compared the effects of high linear energy transfer (LET) fast neutrons on the induction of apoptosis and reduction of neurogenesis in the hippocampus of adult ICR mice with those of low-LET (60)Co gamma-rays, to evaluate the relative biological effectiveness (RBE) of fast neutrons in the adult hippocampal dentate gyrus (DG).
MATERIALS AND METHODS: The mice were exposed to 35 MeV fast neutrons or (60)Co gamma-rays. We evaluated acutely the incidence of apoptosis and expression of Ki-67 (a protein marker for cell proliferation originally defined by the monoclonal antibody Kiel-67) and doublecortin (DCX: an immature progenitor neuron marker) in the hippocampus after a single whole-body irradiation.
RESULTS: The number of terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labelling (TUNEL)-positive apoptotic nuclei in the DG increased and both Ki-67- and DCX-positive cells declined in a dose-dependent pattern, with fast neutrons or gamma-rays. In the hippocampus, which showed an apoptosis frequency between 2 and 8 per DG, the RBE of fast neutrons was approximately 1.9. Additionally, the inhibitory effects of fast neutrons on the expression frequencies of Ki-67 (4-8) and DCX (8-32) were approximately 3.2 and 2.5 times, respectively, the effects of gamma-rays at the same dose.
CONCLUSIONS: Increased apoptotic cell death and decreased neurogenesis in the hippocampal DG were seen in a dose-dependent pattern after exposure to fast neutrons and gamma-rays. In addition, the different rate of hippocampal neurogenesis between different radiation qualities may be an index of RBE.
URL: http://www.ncbi.nlm.nih.gov/pubmed/20470197
Author: V. Bebeshko, D. Bazyka, K. Loganovsky et al.
Reference: Contributed papers to The International Conference “Twenty years after Chornobyl accident future outlook”, April 24–26, Kyiv, Ukraine. — Kyiv: HOLTEH, 2006. — P. 13–19.
Keywords: aging, DNA, immune function, nervous system effects
Abstract: Radiation accelerated aging might be a model of senescence in humans. Natural (normal) aging is a complex temporal process. Radiation is a phenomenon, which, by influencing cell structure and function, changes that process at the molecular and genetic level. A relation of aging and Ionizing Radiation (IR) could be demonstrated by involvement of similar mechanisms, e.g. free radical reactions, DNA repair, changes of immune function, altered lipid metabolism, nervous system effects, etc.
Concepts of immanent and interactional ambivalence (electron donor-acceptor dichotomy) of free radicals in their reactivity, and of free-radical ambivalence in biochemical processes, can be used to analyze free-radical function in normal and pathologic conditions including aging after IR exposure. Prospective epidemiological studies of atomic bomb survivors revealed IR significantly increased mortality for causes other than cancer. Results do not support claims survivors exposed to low IR doses live longer than comparable unexposed individuals. Whether exposure to low dose IR is a risk factor for accelerated aging and neurodegeneration is still unanswered and the biological mechanisms involved unknown. We propose: 1) exposure to low dose IR is a risk factor for accelerated aging and neurodegeneration; 2) heterogeneous pathogenetic factors contribute to the acceleration. International efforts to organize studies to test these hypotheses are of significance for radiation medicine and gerontology.
URL: http://topreferat.znate.ru/docs/index-1478.html
Author: N.A. Hellström, T. Björk-Eriksson, K. Blomgren, H.G. Kuhn
Reference: Stem Cells. ― 2009. ― Vol. 27, № 3. ― P. 634–641.
Keywords: CNS, radiotherapy, hippocampal neurogenesis, SVZ
Abstract: Radiation therapy is a widely used treatment for malignant central nervous system tumors. Mature neurons are terminally differentiated, whereas stem and progenitor cells have a prominent proliferative capacity and are therefore highly vulnerable to irradiation. Our aim was to investigate how cranial radiation in young rats would affect stem/progenitor cells in the two niches of adult neurogenesis, the subventricular zone (SVZ) and the dentate gyrus of the hippocampal formation. Nine weeks after irradiation we found that in irradiated animals, hippocampal neurogenesis was reduced to 5% of control levels. Similarly, the numbers of actively proliferating cells and radial glia-like stem cells (nestin+/glial fibrillary acidic protein [GFAP]+) in the dentate gyrus were reduced to 10% and 15% of control levels, respectively. In the irradiated olfactory bulb, neurogenesis was reduced to 40% of control levels, and the number of actively proliferating cells in the SVZ was reduced to 53% of control levels. However, the number of nestin+/GFAP+ cells in the SVZ was unchanged compared with controls. To evaluate the immediate response to the radiation injury, we quantified the amount of proliferation in the SVZ and dentate gyrus 1 day after irradiation. We found an equal reduction in proliferating cells both in dentate gyrus and SVZ. In summary, we show an initial response to radiation injury that is similar in both brain stem cell niches. However, the long-term effects on stem cells and neurogenesis in these two areas differ significantly: the dentate gyrus is severely affected long-term, whereas the SVZ appears to recover with time.
URL: http://www.ncbi.nlm.nih.gov/pubmed/19056908
Author: P. Lestaevel, E. Romero, B. Dhieux et al.
Reference: Toxicology. — 2009. — Vol. 258, № 1. — P. 1–9.
Keywords: uranium, chemiotoxicity, radiotoxicity, neurological disturbances
Abstract: Uranium is not only a heavy metal but also an alpha particle emitter. The main toxicity of uranium is expected to be due to chemiotoxicity rather than to radiotoxicity. Some studies have demonstrated that uranium induced some neurological disturbances, but without clear explanations. A possible mechanism of this neurotoxicity could be the oxidative stress induced by reactive oxygen species imbalance. The aim of the present study was to determine whether a chronic ingestion of uranium induced anti-oxidative defence mechanisms in the brain of rats. Rats received depleted (DU) or 4% enriched (EU) uranyl nitrate in the drinking water at 2mg(-1)kg(-1)day(-1) for 9 months. Cerebral cortex analyses were made by measuring mRNA and protein levels and enzymatic activities. Lipid peroxidation, an oxidative stress marker, was significantly enhanced after EU exposure, but not after DU. The gene expression or activity of the main antioxidant enzymes, i.e. superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), increased significantly after chronic exposure to DU. On the contrary, oral EU administration induced a decrease of these antioxidant enzymes. The NO-ergic pathway was almost not perturbed by DU or EU exposure. Finally, DU exposure increased significantly the transporters (Divalent-Metal-Transporter1; DMT1), the storage molecule (ferritin) and the ferroxidase enzyme (ceruloplasmin), but not EU. These results illustrate that oxidative stress plays a key role in the mechanism of uranium neurotoxicity. They showed that chronic exposure to DU, but not EU, seems to induce an increase of several antioxidant agents in order to counteract the oxidative stress. Finally, these results demonstrate the importance of the double toxicity, chemical and radiological, of uranium.
URL: http://www.ncbi.nlm.nih.gov/pubmed/19154773
Author: D. Marazziti, S. Baroni, M. Catena-Dell’Osso, et al.
Reference: Curr Med Chem. —2012. — Vol. 19, №12. — P. 1864–1869.
Keywords: cancer, non-cancer diseases, pathophysiology
Abstract: Radiation exposure leads to an increased risk for cancer and, possibly, additional ill-defined non-cancer risk, including atherosclerotic, cardiovascular, cerebro-vascular and neurodegenerative effects. Studies of brain irradiation in animals and humans provide evidence of apoptosis, neuro-inflammation, loss of oligo-dendrocytes precursors and myelin sheaths, and irreversible damage to the neural stem compartment with long-term impairment of adult neurogenesis. With the present paper we aim to present a comprehensive review on brain effects of radiation exposure, with a special focus on its impact on cognitive processes and psychological functions, as well as on their possible role in the pathophysiology of different psychiatric disorders.
URL: http://www.ncbi.nlm.nih.gov/pubmed/22376039
Author: S. Volovik, K. Loganovsky, D. Bazyka et al.
Reference: Contributed papers to The International Conference “Twenty years after Chornobyl accident future outlook”, April 24–26, 2006, Kyiv, Ukraine. — Kyiv: HOLTEH. — P. 114–116.
Author: E.J. Bromet, D. Goldgaber, G. Carlson et al.
Reference: Arch. Gen. Psychiatry. — 2000. — № 57. — P. 563–571.
Keywords: in utero infants, Kyiv, behavioral mental disorders
Abstract: Background The psychological effects of technological disasters have rarely been studied in children. This study assessed the aftermath of the 1986 Chornobyl disaster in children evacuated to Kyiv from the contaminated zone surrounding the nuclear power facility.
Methods In 1997, we evaluated three hundred 10- to 12-year-old children in Kyiv who were in utero or infants at the time of the disaster and who had resided near Chornobyl (evacuees) and 300 sex-matched homeroom classmates who had never lived in a radiation-contaminated area. Response rates were 92% (evacuees) and 85% (classmates). Data were obtained from children, mothers, and teachers using standard measures of well-being and risk factors for childhood psychopathology. The children also received physical examinations and basic blood tests.
Results The evacuees and classmates perceived their mental health similarly except for Chornobyl-related anxiety symptoms and perceived scholastic competence. No differences were found on the Iowa Conners’ Teacher Rating Scale. Although the physical examination and blood test results were normal, the evacuee mothers rated their children’s well-being as significantly worse, especially with respect to somatic symptoms on the Children’s Somatization Inventory and Child Behavior Checklist. The most important risk factors for these ratings were maternal somatization and Chornobyl-related stress.
Conclusions Given the multiple stressful experiences to which evacuee families were exposed, the small differences in the children’s self-reports suggest that there are protective factors in the lives of these children. The trauma experienced by the mothers was reflected in their perceptions of their children’s well-being, particularly somatic symptoms, but was not transmitted to the children themselves.
URL: http://archpsyc.jamanetwork.com/article.aspx?articleid=481617
Author: A.C. Huizink, D.M. Dick, E. Sihvola et al.
Reference: Acta Psychiatr Scand. — 2007. — Vol. 116, № 6. — P. 438–446.
Keywords: prenatal stress, behavioural and neuromotor development, testosterone
Abstract: BACKGROUND: Animal research suggests a programming effect of prenatal stress in the fetal period, resulting in disruptions in behavioural and neuromotor development. Physiological changes that mediate these effects include alterations in the hypothalamic-pituitary-adrenal axis and in testosterone levels. This human study focuses on changes related to these physiological systems after prenatal stress exposure.
METHODS: We examined the potential effect of prenatal stress associated with the Chernobyl disaster in an ongoing genetic epidemiological study in Finland. One birth cohort of twins (n = 121 twin pairs) was exposed in utero to maternal stress, and their saliva cortisol and testosterone levels at age 14 were compared with twins (n = 157 twin pairs) born one year later.
RESULTS: Cortisol levels in both sexes and testosterone levels among females were significantly elevated after prenatal exposure to maternal stress from the second trimester onwards, compared to reference groups of non-exposed adolescents. Exposure explains 3% of variance (p<0.05) in cortisol levels and 18% of variance in testosterone levels (p<0.001). No significant differences were found for exposure from either first or third trimester onwards.
CONCLUSION: Our results suggest that prenatal exposure to maternal stress in the second trimester of pregnancy may have resulted in prenatal programming of physiological systems relating to cortisol and testosterone levels.
URL: http://www.ncbi.nlm.nih.gov/pubmed/18365332
Author: A.C. Huizink, M. Bartels, R.J. Rose et al.
Reference: J. Epidemiol. Community Health. — 2008. — Vol. 62, № 4. — P. e5
Keywords: Adolescent; Chernobyl Nuclear Accident; Glucocorticoids; Prenatal Exposure Delayed Effects;
Testosterone
Abstract: Background—Animal research suggests a programming effect of prenatal stress in the fetal period, resulting in disruptions in behavioral and neuromotor development. Physiological changes that mediate these effects include alterations in the hypothalamic-pituitary-adrenal axis and in testosterone levels. This human study focuses on changes related to these physiological systems after prenatal stress exposure.
Methods— We examined the potential effect of prenatal stress associated with the Chernobyl disaster in an ongoing genetic epidemiological study in Finland. One birth cohort of twins (n= 121 twin pairs) was exposed in utero to maternal stress, and their saliva cortisol and testosterone levels at age 14 were compared with twins (n = 157 twin pairs) born one year later.
Results—Cortisol levels in both sexes and testosterone levels among females were significantly elevated after prenatal exposure to maternal stress from the second trimester onwards, compared to reference groups of non-exposed adolescents. Exposure explains 3 percent of variance (p<0.05) in cortisol levels and 18 percent of variance in testosterone levels (p< 0.001). No significant differences were found for exposure from either first or third trimester onwards.
Conclusion—Our results suggest that prenatal exposure to maternal stress in the second trimester of pregnancy may have resulted in prenatal programming of physiological systems relating to cortisol and testosterone levels. (full text available on web)
URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562331/pdf/nihms34067.pdf
Author: E. Picano, E. Vano, L. Domenici et al.
Reference: BMC Cancer. — 2012. — Vol. 12, №1. — P. 157.
Keywords: Brain cancer; Cognitive effects; Interventional cardiologist; Radiation exposure; Risk
Abstract: Background: According to a fundamental law of radiobiology (“Law of Bergonié and Tribondeau”, 1906), the brain is a paradigm of a highly differentiated organ with low mitotic activity, and is thus radio-resistant. This assumption has been challenged by recent evidence discussed in the present review.
Results: Ionizing radiation is an established environmental cause of brain cancer. Although direct evidence is lacking in contemporary fluoroscopy due to obvious sample size limitation, limited follow-up time and lack of focused research, anecdotal reports of clusters have appeared in the literature, raising the suspicion that brain cancer may be a professional disease of interventional cardiologists. In addition, although terminally differentiated neurons have reduced or mild proliferative capacity, and are therefore not regarded as critical radiation targets, adult neurogenesis occurs in the dentate gyrus of the hippocampus and the olfactory bulb, and is important for mood, learning/memory and normal olfactory function, whose impairment is a recognized early biomarker of neurodegenerative diseases. The head doses involved in radiotherapy are high, usually above 2 Sv, whereas the low-dose range of professional exposure typically involves lifetime cumulative whole-body exposure in the low-dose range of < 200 mSv, but with head exposure which may (in absence of protection) arrive at a head equivalent dose of 1 to 3 Sv after a professional lifetime (corresponding to a brain equivalent dose around 500 mSv).
Conclusions: At this point, a systematic assessment of brain (cancer and non-cancer) effects of chronic low-dose radiation exposure in interventional cardiologists and staff is needed.
URL: http://www.biomedcentral.com/1471-2407/12/157 (full text on web)
