Assess the annual effective dose and contribute to risk of lung cancer caused by internal radon 222 in 22 regions of Tehran, Iran using geographic information system

Radon gas is one of the most influential sources of indoor exposure. All its physical properties together make it a significant risk factor for lung cancer in the population. The research aims are outlined as (1) to measure the radon concentration in Tehran city and compare results with the international standards (2) to determine spatial distribution of radon gas concentration using Geographical Information System (GIS) software and (3) to estimate the annual effective dose and potential risk of lung cancer by radon-222 in Tehran city. In this study, 800 Alpha Track detectors were installed in houses in 22 regions of Tehran city and retrieved after 3 months. The measurements were repeated for spring and summer and autumn seasons. The annual effective dose and risk of lung cancer were assessed using standard equations. Data were analyzed using SPSS 20. Result showed the minimum and maximum radon concentration were observed in and Ghalee-kobra (0.13 Bq.m-3) and Charbagh-ponak district (661.11 Bq.m-3) respectively. There was no observed relationship between radon concentration and houses' model, cracking condition and constructionn materials. Expectedly, the storehouses and basements had significantly higher (P = 0.016) radon concentration than occupied rooms. The min and max of the estimated annual effective dose were 0.65 and 2.03 mSv, respectively. Result showed that around 5 of the sampling sites had higher level of radon than the maximum allowed by EPA. A rough estimation of the expected radon-attributed lung cancer incidences yielded approximately 5958 cases in the total population of Tehran every year. In view of the growing trend in cancer incidences, appropriate measures addressing radon should be undertaken in areas of increased exposure to this noble gas. © 2020 Springer Nature Switzerland AG

Post-stroke dementia - a comprehensive review

Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing

Impact of Cerebral Microbleeds in Stroke Patients with Atrial Fibrillation

OBJECTIVES: Cerebral microbleeds are associated with the risks of ischemic stroke and intracranial hemorrhage, causing clinical dilemmas for antithrombotic treatment decisions. We aimed to evaluate the risks of intracranial hemorrhage and ischemic stroke associated with microbleeds in patients with atrial fibrillation treated with Vitamin K antagonists, direct oral anticoagulants, antiplatelets, and combination therapy (i.e. concurrent oral anticoagulant and antiplatelet) METHODS: We included patients with documented atrial fibrillation from the pooled individual patient data analysis by the Microbleeds International Collaborative Network. Risks of subsequent intracranial hemorrhage and ischemic stroke were compared between patients with and without microbleeds, stratified by antithrombotic use. RESULTS: A total of 7,839 patients were included. The presence of microbleeds was associated with an increased relative risk of intracranial hemorrhage (aHR 2.74, 95% confidence interval 1.76 - 4.26) and ischemic stroke (aHR 1.29, 95% confidence interval 1.04 - 1.59). For the entire cohort, the absolute incidence of ischemic stroke was higher than intracranial hemorrhage regardless of microbleeds burden. However, for the subgroup of patients taking combination of anticoagulant and antiplatelet therapy, the absolute risk of intracranial hemorrhage exceeded that of ischemic stroke in those with 2-4 microbleeds (25 vs 12 per 1,000 patient-years) and ≥11 microbleeds (94 vs 48 per 1,000 patient-years). INTERPRETATION: Patients with atrial fibrillation and high burden of microbleeds receiving combination therapy have a tendency of higher rate of intracranial hemorrhage than ischemic stroke, with potential for net harm. Further studies are needed to help optimize stroke preventive strategies in this high-risk group. This article is protected by copyright. All rights reserved

Cognitive state following stroke: the predominant role of preexisting white matter lesions.

Stroke is a major cause of cognitive impairment and dementia in adults, however the role of the ischemic lesions themselves, on top of other risk factors known in the elderly, remains controversial. This study used structural equation modeling to determine the respective impact of the new ischemic lesions' volume, preexisting white matter lesions and white matter integrity on post stroke cognitive state.Consecutive first ever mild to moderate stroke or transient ischemic attack patients recruited into the ongoing prospective TABASCO study underwent magnetic resonance imaging scans within seven days of stroke onset and were cognitively assessed one year after the event using a computerized neuropsychological battery. The volumes of both ischemic lesions and preexisting white matter lesions and the integrity of the normal appearing white matter tissue were measured and their contribution to cognitive state was assessed using structural equation modeling path analysis taking into account demographic parameters. Two models were hypothesized, differing by the role of ischemic lesions' volume.Structural equation modeling analysis of 142 patients confirmed the predominant role of white matter lesion volume (standardized path coefficient β =  -0.231) and normal appearing white matter integrity (β =  -0.176) on the global cognitive score, while ischemic lesions' volume showed no such effect (β = 0.038). The model excluding the ischemic lesion presented better fit to the data (comparative fit index 0.9 versus 0.092).Mild to moderate stroke patients with preexisting white matter lesions are more vulnerable to cognitive impairment regardless of their new ischemic lesions. Thus, these patients can serve as a target group for studies on cognitive rehabilitation and neuro-protective therapies which may, in turn, slow their cognitive deterioration

Structural equation models for the prediction of cognitive state after one year.

<p>Subtext: The numbers on the arcs represent the contribution of each parameter to its neighbor. * <i>p</i><0.05 **<i>p</i><0.001. Abbreviations: ILV, ischemic lesions' volume; WML, white matter lesions; NAWM, normal appearing white matter.</p

Correlation coefficients for the associations between ischemic lesions and white matter lesion volumes, white matter tissue integrity parameters and cognitive domain scores after one year.

<p>Correlation coefficients for the associations between ischemic lesions and white matter lesion volumes, white matter tissue integrity parameters and cognitive domain scores after one year.</p