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2017| October-December | Volume 8 | Issue 4
Online since
January 8, 2018
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REVIEW ARTICLE
Mobile phone use and cancer: Does dose really matter?
SMJ Mortazavi, Kaushala P Mishra
October-December 2017, 8(4):165-167
DOI
:10.4103/jrcr.jrcr_39_17
The past decades have witnessed rapid evolution of telecommunication technology and wireless devices. Due to these rapid advances, cell phone usage has remarkably increased the level of human exposure to radiofrequency-electromagnetic fields (RF-EMFs). In the past, it was widely believed that, RF-EMF, in contrast to ionizing radiation, does not have enough energy for ionizing atoms and hence does not cause DNA damage which can lead to cancer. However, substantial evidence now indicates that RF-EMFs increase the reactive oxygen species production and DNA damages which play an important role in the initiation and progression of cancer. Currently, there is no widely accepted answer to this question whether there is a relationship between exposure to RF-EMFs from cell phones and cancer incidence and mortality. Although it seems that this issue is a long-term unsolved problem, new studies have raised new concerns over the safety of mobile phones. Mortazavi have previously studied the health effects of cellular phones, mobile base stations, and Wi-Fi. They have also reviewed reports claiming no link between exposure to RF and brain cancer. They found that in many cases there were large errors and/or major shortcomings in these articles. They have also reported that current controversies may be caused by the key parameter of the large difference in the magnitude of exposures to RF-EMFs in different studies. In this light, in a similar pattern with ionizing radiation, a nonlinear J-shaped dose–response relationship for the carcinogenesis of nonionizing RF-EMF is introduced.
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ORIGINAL ARTICLES
Thyroid nodule prevalence among young residents in the evacuation area after fukushima daiichi nuclear accident: Results of preliminary analysis using the official data
Suminori Akiba, Athira Nandakumar, Kenta Higuchi, Mayumi Tsuji, Futoshi Uwatoko
October-December 2017, 8(4):174-179
DOI
:10.4103/jrcr.jrcr_42_17
Introduction:
The nuclear accidents at Fukushima Daiichi Nuclear Power Plant released more than 10 EBq (exabecquerel) of the radionuclides into the atmosphere. A primary health concern after the nuclear accident is the internal exposure of children to radioactive iodines, which are known to accumulate in the thyroid, and to cause neoplasm. Fortunately, studies conducted so far have shown that the thyroid doses from internal exposure to
131
I were low, and therefore, any excess risk of thyroid cancer among residents is considered unlikely to be detected in the future.
Data and Analysis:
Approximately half a year after the accident, the Fukushima Health Management Survey was started. It includes the thyroid screening survey using ultrasonography and a program to estimate the individual radiation dose of residents and evacuees.
Results and Discussions:
The first-round thyroid survey, which was conducted during the period 2011–2013, covered 300,476 young residents, approximately 82% of residents eligible for the survey, and found thyroid nodules in 3990 examinees. The prevalence of nodules in the evacuation zone was similar to that in the nonevacuation zone. The second-round survey, which was conducted during the period 3–6 years after the accident, detected 3788 participants with thyroid nodules among 270,511 examinees (approximately 71% of eligible residents). The prevalence of thyroid nodules in the evacuation zone was significantly higher than that in the rest of area (relative risk = 1.32; 95% confidence interval = 1.19, 1.45).
Conclusion:
Further studies are necessary to evaluate the scientific significance of present findings.
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TECHNICAL REPORT
Technical note on cytokinesis-arrested binucleated cell and micronucleus assay
Karthik Kanagaraj, Venkateswarlu Raavi, Shangamithra Visweswaran, Tamizh Gnanasekaran Selvan, Shanmugapriya Dhanashekaran, Venkatachalam Perumal
October-December 2017, 8(4):180-185
DOI
:10.4103/jrcr.jrcr_40_17
Conventionally, many biomarkers are being in use as a measure to genotoxicity in occupational exposure to chemicals, pesticides, radiation, and drug screening. Of which, the micronucleus assay is a preferred choice for many of those applications owing to its simplicity and rapidity. The assay methodology has evolved in cell preparations, staining, and scoring methods: from quantifying the DNA damage in mononucleated cells and binucleated cells; solid (Giemsa) and fluorescence staining (propidium iodide/DAPI); and manual and automated microscopy scoring and flow cytometry. Despite the advantages, preparation of cells with good morphology to interpret DNA damage from a different type of cells remains a challenge in particular for laboratory being the processes of developing the assay. Therefore, the aim of the present report was to explain the micronuclei (MN) assay and means to overcome the troubleshoot for reliable outcome measure using cytokinesis-arrested micronucleus (CBMN) assay from suspension and adherent cultures.
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MEETING REPORT
Recent advances in radiation research for human health and environment
Amit Kumar, Neena G Shetake, Manjoor Ali, Sagar Balla, Rakhee Yadav, Badri N Pandey, Kaushala P Mishra
October-December 2017, 8(4):186-191
DOI
:10.4103/jrcr.jrcr_41_17
The 1
st
International Conference on Radiation Research: Impact on Human Health and Environment (2016) and First Biennial Meeting of Society for Radiation Research was organized at Bhabha Atomic Research Centre in Mumbai (India). Recent developments in molecular, translational, and clinical radiobiology were discussed among basic and translational scientists as well as clinicians. The meeting has covered the topics ranging from the most recent insight into the paradigm shift from DNA-based radiation health effects (epigenetics), radiation biology from laboratory clinic, radiobiologically relevant redox metabolism, hypoxia, stem cell biology, hyperthermia to advances in dose deposition, and understanding the molecular biological effects of high linear energy transfer (LET) radiation. Mechanism of radiobiological effects of actinides, and the search for novel radiosensitizers, radiation countermeasures, and efficient actinide decorporation agents were discussed for further improvement in cancer radiotherapy, radiation protection, and medical management of internal contamination in humans. This report summarizes the key points of recent observations/results presented in the meeting, and highlights their importance in view of human health and environment. This document would also help in understanding the significance of synergistic interaction among radiation researchers, scientists, clinicians, medical physicists, and radiation environmentalists for harnessing the real potential of radiation/radioactivity for better care of human health and environment.
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EDITORIAL
Necessity of reference dosimetry, periodic quality assurance, and dosimetry audit in preclinical and radiobiology research
SD Sharma
October-December 2017, 8(4):163-164
DOI
:10.4103/jrcr.jrcr_44_17
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ORIGINAL ARTICLES
Beta radiation induces apoptosis in human histiocytic lymphoma cells
Chandan Kumar
October-December 2017, 8(4):168-173
DOI
:10.4103/jrcr.jrcr_35_17
Objective:
Lu-177 has a great potential for use as theranostics radiopharmaceuticals for management of cancer, evidenced by its increasing use over the past decade in nuclear medicine. The detail mechanisms of cell toxicity induced by the beta-radiation emitted from Lu-177 are not well understood. Hence, to explore the lurking mechanism of cell death, different parameters were assessed after treatment of human histiocytic lymphoma cells (U937) with Lu-177.
Materials and Methods:
U937 cells (1 × 10
6
) were exposed to 3.7 and 37 MBq of Lu-177 and incubated for 24 and 48 h in humidified CO
2
incubator. The cell viability and apoptosis were estimated in treated and control cells by trypan blue dye exclusion and electrophoretic DNA ladder assay, respectively. Reverse transcriptase polymerase chain reaction was carried out to study the expression of anti-apoptotic genes.
Results:
It was found that the cell death and apoptosis were high in the cells which were exposed for a longer duration of time with 37MBq of Lu-177. These results were further confirmed by observation of downregulation of anti-apoptotic genes such as
BCL-2
and
BCL
XL
.
Conclusion:
It is concluded from the study that the Lu-177 induced apoptotic cell death in human histiocytic lymphoma cells by downregulation of anti-apoptotic genes.
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Online since 29
th
February,2016