Radioactive Contamination Of Natural Biological Systems: Oxidative Balance And Genetic Stability

The global demand for nuclear energy grows, and so do the risks of an accidental release of nuclear products into the environment. Therefore, understanding the health and ecological effects of contamination by radionuclides should be of great interest for biomedical specialists and the public. Empirical studies unequivocally show that high doses of ionizing radiation (IR) shift the redox-balance of many biological systems and increase the rates of genetic errors. However, the effects of chronic low doses of radiation vary significantly between tissues and between species. The present dissertation comprises the results of experimental and meta-analytical research of a variety of biological effects of environmental contamination by radioactive isotopes. In the review part (Chapter 1), I performed a rigorous literature analysis of the environmental consequences of the three most serious nuclear accidents – the Fukushima Daiichi nuclear power plant (NPP) accident in Japan (2011); meltdown at the Chernobyl NPP in 1986; and the explosion at the Mayak plutonium production site (both former USSR) in 1957. The results of the meta-analysis demonstrate significant effects of the low ( In the experimental part of this thesis (Chapter 2&3), I presented the results of several tests, by which I aimed to detect the detrimental genetic effects of low dose IR. I tested for the presence of radiation-induced damage in DNA and related that to radionuclide body burdens and fitness of a model animal. The bank vole was used as a vertebrate model and the wild downy dragonfly as an invertebrate model. Both species were sampled in the Chernobyl Exclusion Zone (CEZ), as it remains significantly contaminated by the biologically effective isotopes: cesium-137 and strontium-90. In the results, I demonstrate that natural variation in comet-visualized DNA damage exceeds the additive effect of damage from ionizing radiation. It was also shown that accounting for morphological co-variates, such as sex and age, and random co-variates, such as sampling period, is important in prediction of genetic damage using the comet assay

Unsupervised learning for detection of possible sexual dimorphism in larvae of Belgica antarctica Jacobs (Diptera, Chironomidae)

Belgica antarctica is one of the two native chironomid species of the Antarctic Peninsula. In this species, adult males and females are considerably different, yet the question of larval sex differences in morphometric parameters remains unanswered. In this paper, we analyze five morphometric parameters: head capsule length, head capsule width, mandible width, mandible length, mentum length of 140 fourth-instar larvae of B. antarctica from seven study plots in the south of Petermann Island, Wilhelm Archipelago, Antarctic Peninsula. To infer possible sexual dimorphism, we use the methods of unsupervised analysis (PCA and hierarchical clusterization). Our results suggest that the selected morphometric features of width and length are highly intercorrelated and cannot differentiate sex in the sampled larvae of B. antarctica

Data on assessment excess lifetime cancer risk and risk of lung cancer from inhalation of Radon 222 in radiotherapy centers in Tehran, Iran

The purpose of the data was to determine excess lifetime cancer risk (ELCR) and risk of lung cancer from inhalation of radon in radiotherapy staff at Tehran radiotherapy Centers in 2015.The concentration of radon gas was extracted from a study done at Tehran radiotherapy centers, and then ELCR and risk of lung cancer were calculated in all centers by standard equations. The excess lifetime cancer risk and risk of lung cancer were 1.89 and 8.46 cases per 100,000 people in radiotherapy centers in Tehran City. The data indicate that the excess lifetime cancer risk and risk of lung cancer in radiotherapy centers are lower than the standard values which presented by UNSCEAR 2000. Keywords: Background radiations, Excess lifetime cancer risk, Risk of lung cancer, Radiotherapy center

Environmental radiation alters the gut microbiome of the bank vole Myodes glareolus

Gut microbiota composition depends on many factors, although the impact of environmental pollution is largely unknown. We used amplicon sequencing of bacterial 16S rRNA genes to quantify whether anthropogenic radionuclides at Chernobyl (Ukraine) impact the gut microbiome of the bank vole Myodes glareolus. Exposure to elevated levels of environmental radionuclides had no detectable effect on the gut community richness but was associated with an almost two-fold increase in the Firmicutes:Bacteroidetes ratio. Animals inhabiting uncontaminated areas had remarkably similar gut communities irrespective of their proximity to the nuclear power plant. Hence, samples could be classified to high-radiation or low-radiation sites based solely on microbial community with >90% accuracy. Radiation-associated bacteria had distinct inferred functional profiles, including pathways involved in degradation, assimilation and transport of carbohydrates, xenobiotics biodegradation, and DNA repair. Our results suggest that exposure to environmental radionuclides significantly alters vertebrate gut microbiota.peerReviewe

Stroke Risk and Antithrombotic Treatment During Follow-up of Patients With Ischemic Stroke and Cortical Superficial Siderosis.

BACKGROUND AND OBJECTIVES In patients with ischemic stroke (IS) or TIA and cortical superficial siderosis (cSS), there are few data regarding the risk of future cerebrovascular events and also about the benefits and safety of antithrombotic drugs for secondary prevention. We investigated the associations of cSS and stroke risk in patients with recent IS or TIA. METHODS We retrospectively analyzed the Microbleeds International Collaborative Network (MICON) database. We selected patients with IS or TIA from cohorts who had MRI-assessed cSS, available data on antithrombotic treatments, recurrent cerebrovascular events [Intracranial hemorrhage -ICrH-, IS, or any stroke (ICrH or IS)], and mortality. We calculated incidence rates (IR) and performed univariable and multivariable Cox regression analyses. RESULTS Of 12.669 patients (mean age 70.4±12.3 years, 57.3% men), cSS was detected in 273 (2.2%) patients. During a mean follow-up of 24±17 months, IS was more frequent than ICrH in both cSS (IR 57.1 versus 14.6 per 1000 patient-years) and non-cSS groups (33.7 versus 6.3 per 1000 patient years). Compared to the non-CSS group, cSS was associated with any stroke on multivariable analysis [IR 83 versus 42 per 1000 patient-years, adjusted HR for cSS 1.62 (95%CI: 1.14-2.28; p=0.006)]. This association was not significant in subgroups of patients treated with antiplatelet drugs (n=6.554) or with anticoagulants (n=4.044). Patients with cSS who were treated with both antiplatelet drugs and anticoagulants (n=1.569) had a higher incidence of ICrH (IR 107.5 vs 4.9 per 1000 patient-years, adjusted HR 13.26; 95%CI: 2.90-60.63; p=0.001) and of any stroke (IR 198.8 vs 34.7 per 1000 patient-years, adjusted HR 5.03; 95%CI: 2.03-12.44; p<0.001) compared to the non-CSS group. DISCUSSION Patients with IS or TIA with cSS are at increased risk of stroke (ICrH or IS) during follow-up; the risk of IS exceeds that of ICrH for patients receiving antiplatelet or anticoagulant treatment alone, but the risk of ICrH exceeds that of IS in patients receiving both treatments. The findings suggest that either antiplatelet or anticoagulant treatment alone should not be avoided in patients with cSS, but combined antithrombotic therapy might be hazardous. Our findings need to be confirmed by randomized clinical trials

Cerebral microbleeds and stroke risk after ischaemic stroke or transient ischaemic attack:a pooled analysis of individual patient data from cohort studies

BACKGROUND Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. METHODS We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. FINDINGS Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19-2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20-1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82-3·29) for intracranial haemorrhage and 1·23 (1·08-1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08-6·72] for intracranial haemorrhage vs 1·47 [1·19-1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36-9·05] vs 1·43 [1·07-1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69-15·81] vs 1·86 [1·23-1·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48-84] per 1000 patient-years vs 27 intracranial haemorrhages [17-41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46-108] per 1000 patient-years vs 39 intracranial haemorrhages [21-67] per 1000 patient-years). INTERPRETATION In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden. FUNDING British Heart Foundation and UK Stroke Association