A study of the protective actions for a hypothetical accident of the Bushehr nuclear power plant at different meteorological conditions.

In this work, protective actions have been studied assuming a hypothetical severe accident of the Bushehr nuclear power plant at different meteorological conditions. Simulations of the atmospheric dispersion of accidental airborne releases were performed using the RASCAL code. Total effective dose equivalent (TEDE) and thyroid dose received by members of the public living within a radius of 40 km around the reactor site were calculated for various atmospheric stability classes and weather conditions. According to the results of the dose assessment and by following the protective action guide of the Environmental Protection Agency (EPA), the critical zone and appropriate protective actions were determined depending on various metrological conditions. It was found that, for atmospheric stability class F and calm weather conditions, the maximum distance from the site of release for which TEDE is greater than the corresponding dose limit and for which sheltering or evacuation response actions are required, is 11 km. For the same weather conditions, the corresponding maximum distance for which iodine prophylaxis is required is 32 km. Based on the present simulations, it can be concluded that the metrological condition has a great influence on the radionuclide atmospheric dispersion and, consequently, on the critical zone where protective actions are required after the assumed accident condition.

Simulation of radionuclide atmospheric dispersion and dose assessment for inhabitants of Tehran province after a hypothetical accident of the Tehran Research Reactor.

Radiological dose assessment is one of the main categories of safety assessment for nuclear reactors and facilities. The radiation risks to the public and to the environment that may arise from these facilities have to be assessed and, if necessary, controlled. The main objective of this paper is the assessment of radiation doses to residents of Tehran province after a hypothetical accident of the Tehran Research Reactor (TRR) including the determination of any protective actions that might be needed for the benefit of people's health. The concentration of radionuclides in air and deposited on the ground surface as a result of a hypothetical radionuclide release from the TRR, following a hypothetical accident scenario, have been calculated by the HYSPLIT computer code. Simulations were performed using selected source terms taken from the TRR Final Safety Analysis Report (FSAR). Meteorological data of the Air Resources Laboratory of the National Oceanic and Atmospheric Administration (NOAA) have been used in these calculations. The simulation results indicate that maximum annual total effective dose equivalent values for the residents of the Tehran province are less than the protective action dose limits. Thus, it is concluded that during this hypothetical accident in the TRR, required safety due to public radiation is achieved and the residents of Tehran province are safe under a TRR accident condition.

The effect of vitamin D supplementation in combination with low-calorie diet on anthropometric indices and androgen hormones in women with polycystic ovary syndrome: a double-blind, randomized, placebo-controlled trial.

PURPOSE: Polycystic ovary syndrome (PCOS) is known as the most common endocrine disorder in reproductive age women. The aim of this studywas to evaluate the effects of vitamin D supplementation in combination with low-calorie diet on anthropometric indices, reproductive hormones and menstrual regularity in overweight and obese PCOS women. METHODS: In this randomized controlled clinical trial, 60 PCOS women with vitamin D insufficiency were randomly assigned to 12 weeks of either (1) weight-loss intervention + 50,000 IU/week oral vitamin D3 or (2) weight-loss intervention + placebo. At the beginning and end of the study, the anthropometric indices, body composition, 25-hydroxyvitamin D, total testosterone, dehydroepiandrosterone sulfate (DHEAS), sex hormone-binding globulin (SHBG) and free androgen index (FAI) were measured and regularity of menses was compared among the two groups. RESULT: After 12-week intervention, median of serum 25-hydroxyvitamin D3 significantly increased from 18.5 (10.75-20) ng/ml to 42.69 (34-53.25) ng/ml in vitamin D group compared to placebo group (p < 001). Moreover, there was a significant improvement in frequency regular menstrual cycle (p = 0.01). Mean of weight, body mass index, fat mass, waist and hip circumference and waist-to-hip ratio significantly decreased in both groups, but was not different between two groups. Mean of total testosterone insignificantly decreased from 0.7 to 0.5 ng/ml in vitamin D group (p = 0.18). In addition, we did not observe significant differences regarding DHEAS, FAI and SHBG between two groups. CONCLUSIONS: In women with PCOS, androgen profile did not change with vitamin D supplementation when combined with low-calorie diet, but menstrual frequency significantly improved. CLINICAL TRIAL REGISTRATION NUMBER: IRCT2016062710826N19.

A new approach to dose estimation and in-phantom figure of merit measurement in BNCT by using artificial neural networks.

In-phantom figures of merit of the radiobiological dose distribution are the main criteria for evaluation of the boron neutron capture therapy (BNCT) plan and neutron beam evaluation. Since in BNCT there are several reactions, which contribute to the total dose of the tissue, the calculation of the dose distribution is complicated and requires lengthy and time-consuming simulations. Any changes in the beam shaping assembly (BSA) design would lead to the change of the neutron/gamma spectrum at exit of therapeutic window. As a result of any changes in the beam spectrum, the dose distribution in the tissue will be altered; therefore, another set of lengthy and time-consuming simulations to recalculate the dose distribution would have to be performed. This study proposes a method that applies artificial neural network (ANN) for quick dose prediction in order to avoid lengthy calculations. This method allows us to estimate the depth-dose distribution and in-phantom figures of merit for any energy spectrum without performing a complete Monte Carlo code (MCNP) simulation. To train the ANNs for modeling the depth-dose distribution, this study used a database containing 500 simulations of the neutron depth-dose distribution and 280 simulations of the gamma depth-dose distribution. The calculations were carried out by the MCNP for various mono-energetic neutrons, ranging from thermal up to 10 MeV energy and 280 gamma energy group, ranging from 0.01 MeV up to 20 MeV, through the SNYDER head phantom which is located at the exit of the BSA. The trained ANN was capable of establishing a map between the neutron/gamma beam energy and the dose distribution in the phantom as an input and a response, respectively. The current method is founded upon the observation that the dose which is released by the beam of composite energy spectrum can be decomposing into the various energy components which make the neutron/gamma spectrum. Therefore, in this procedure the neutron/gamma energy spectrum was converted into several energy groups and dose response of each group was predicted by the trained ANN. Total dose distribution of the entire spectrum is equal to summation of dose response of each group. If the neutron/gamma spectrum as an input changes, the dose response of that as an output can be predicted by the trained ANN in no time rather than hours or days by MCNP simulations. To check the validity of this method, this study compared full calculation of the depth-dose distribution with prediction of ANN for that. The result of this comparison shows that artificial neural networks model the dose distribution in phantom successfully and result in a great accurate prediction.

[Implication of the neuropeptides methionine enkephalin, neurotensin and somatostatin of the caudal trigeminal nucleus in the experimental migraine]. / Implicación de los neuropéptidos metionina-encefalina, neurotensina y somatostatina del núcleo caudal del trigémino en la migraña experimental.

INTRODUCTION: Primary peptidergic sensory neurons of the trigeminal ganglion that innervate the cerebral dura have been involved in the pathogenesis of headache, including the migraine. In addition, it is known that nociceptive central processes of the trigeminal neurons terminate in the caudal trigeminal nucleus. Moreover, the electrical stimulation of the trigeminal ganglion has been used as an experimental model in order to study the vascular headache, including the migraine. AIM: To study whether there is or not a decrease of the immunoreactivity for methionine enkephalin, somatostatin and neurotensin in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion. MATERIAL AND METHODS: The trigeminal ganglia of Wistar albino rats of both sexes were electrically stimulated (frequency, 5 Hz; duration, 5 ms; intensity, 0,8 1.4 mA) and unilaterally for five minutes. Sections of the medulla oblongata containing the caudal trigeminal nucleus were obtained and processed for immunocytochemistry, in which specific antibodies were used against methionine enkephalin, neurotensin and somatostatin 28. RESULTS: In stimulated animals, we observed a decrease in the immunoreactivity for the three neuropeptides studied in the stimulated (ipsilateral) side, in comparison with the not stimulated side (contralateral). In control animals (not stimulated) the degree of the immunoreactivity was the same on both sides. CONCLUSIONS: 1. The decrease of the immunoreactivity in the ipsilateral side (stimulated) suggests that methionine enkephalin, neurotensin and somatostatin 28 are released in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion; 2. Methionine enkephalin and somatostatin 28 could act in the caudal trigeminal nucleus as inhibitors (with antinociceptive action) of another released exciters neuropeptides (with nociceptive action); and 3. These data will allow in the future to try new therapeutic strategies (e.g., the inhibition of the receptors implicated.), in order to alleviate certain headaches.

Implicación de los neuropéptidos metionina-encefalina, neurotensina y somatostatina del núcleo caudal del trigémino en la migraña experimental / Implication of the neuropeptides methionine-enkephalin, neurotensin and somatostatin of the caudal trigeminal nucleus in the experimental migraine

Introducción. Las neuronas peptidérgicas sensoriales primarias del ganglio del trigémino que inervan la duramadre se han involucrado en la patogénesis de la cefalea, incluida la migraña. También se sabe que las terminaciones nociceptivas de las neuronas trigeminales finalizan en el núcleo caudal del trigémino, y que la estimulación eléctrica del ganglio del trigémino se ha utilizado como modelo experimental para estudiar la cefalea de origen vascular, incluyendo la migraña. Objetivo. Estudiar si hay disminución de la inmunorreactividad para la metionina-encefalina, somatostatina y neurotensina en el núcleo caudal del trigémino tras estimular eléctricamente el ganglio del trigémino. Material y métodos. El ganglio del trigémino de ratas Wistar albinas de ambos sexos se estimuló eléctricamente (frecuencia, 7,5 Hz; duración, 5 ms; intensidad, 0,8-1,4 mA) y unilateralmente durante cinco minutos. Una vez obtenidas las secciones del bulbo raquídeo que contienen el núcleo caudal del trigémino, se realizó una técnica inmunocitoquímica en la que se utilizaron anticuerpos específicos contra la metionina-encefalina, neurotensina y somatostatina-28. Resultados. En los animales que se estimularon observamos una disminución de la inmunorreactividad para los tres neuropéptidos en el lado estimulado (ipsilateral) con respecto al no estimulado (contralateral). En los animales controles (no estimulados), el grado de inmunorreactividad observado fue idéntico en ambos lados. Conclusiones. 1. La disminución de la inmunorreactividad en el lado ipsilateral (estimulado) indica que la metionina-encefalina, neurotensina y somatostatina-28 se liberan en el núcleo caudal del trigémino tras estimular eléctricamente el ganglio del trigémino; 2. La metionina-encefalina y la somatostatina-28 en el núcleo caudal del trigémino podrían actuar como inhibidores (con acción antinociceptiva) de otros neuropéptidos que se liberan y que tienen una acción excitadora (con acción nociceptiva); y 3. Estos datos permitirán ensayar nuevas estrategias terapéuticas en el futuro (ej., inhibición de los receptores implicados...) con la finalidad de tratar ciertas cefaleas (AU)

Depletion of substance P, neurokinin A and calcitonin gene-related peptide from the contralateral and ipsilateral caudal trigeminal nucleus following unilateral electrical stimulation of the trigeminal ganglion; a possible neurophysiological and neuroanatomical link to generalized head pain.

Primary trigeminal neurons of the trigeminal ganglion (TG) innervate major parts of the face and head, including the dura. Electrical stimulation of the TG at specific parameters, can activate its nociceptive neurons and may serve as an experimental pain model. Markowitz [J. Neurosci. 7 (1987) 4129] reported that electrical stimulation of the trigeminal ganglion (TG) causes extravasation of plasma proteins from venules of the trigeminally innervated domain possibly due to the release of vasoactive substances. Neurogenic inflammation (vasodilatation, plasma protein extravasation, release of vasoactive peptides) in dura may serve as one of the possible pathomechanisms underlying vascular head pain [Moskowitz, Ann. Neurol. 16 (1984) 157]. We performed a unilateral electrical stimulation (7.5 Hz, 5 ms, 0.8-1.4 mA for 5 min) of the TG in rat, to induce a neurogenic inflammation in the peripheral trigeminal domain including the dura, looking for calcitonin gene related peptide (CGRP), substance P (SP) and neurokinin A (NKA) immunoreactivity (IR) in the caudal trigeminal nucleus (CTN) into which massive central trigeminal processes terminate. Here, we show patchy depletion(s) of CGRP-, SP- and NKA-IRs in the contralateral CTN of the rat in addition to their ipsilateral depletion. Such depletion is due to the release of these neuropeptides in the CTN leading to the activation of bilateral trigeminal nociceptive pathway. These data afford the possibility that under specific frequencies (which may roughly correlate to the intensity of the painful stimulus) and/or specific intensities (may correlate to specific areas of the peripheral trigeminal domain) of stimulation, activation of one side of the TG may activate bilateral trigeminal nociceptive pathway leading to the perception of an ill localized/generalized pain or headache rather than a unilateral one.

Modificaciones en la distribución de neuropéptidos en el núcleo caudal del trigémino tras estimulación eléctrica del ganglio del trigérnino: modelo experimental de migraña / Changes in neuropeptide distribution in the caudal trigeminal nucleus following electrical stimulation of the trigeminal ganglion: an experimental migraine model

Con el fin de inducir algunas de las alteraciones que ocurren durante los ataques de migraña, hemos estimulado eléctricamente y unflateralmente el ganglio del trigémino de la rata, durante 5-30 minutos, para conocer en el núcleo caudal del trigémino las modifícaciones que aparecen en la distribución de los neuropéptidos sustancia P, neuroquinina A y péptido relacionado con el gen de la calcitonina. Una vez realizada la estimulación y la técnica inmunocitoquímica, observamos en secciones seriadas del núcleo caudal del trigémino ipsilateral una disminución signifícativa, con respecto al lado contralateral, de las terminaciones nerviosas inmunorreactivas que contienen a los neuropéptidos mencionados. Estas observaciones indican que durante los ataques de migraña, los tres neuropéptidos se liberan conjuntamente en el núcleo caudal del trigémino en donde actuarían a nivel de la primera sinapsis de la vía sensorial trigeminal como neurotransmisores y/o neuromoduladores de la información nociceptiva. (AU)

Simultaneous depletion of neurokinin A, substance P and calcitonin gene-related peptide from the caudal trigeminal nucleus of the rat during electrical stimulation of the trigeminal ganglion.

The central terminals of the primary sensory trigeminal ganglion (TG) neurons projecting into the caudal trigeminal nucleus (CTN) of the rat exhibit neurokinin A (NKA)-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)-immunoreactivities (IRs). We stimulated the TG in the rat to induce some of the alterations which might occur during migraine (neurogenic inflammation). Under a stereotaxic apparatus and by means of a bipolar electrode, one-side TG of the animals were electrically stimulated (7.5 Hz, 5 ms, 0.8-1. 4 mA) with square pulses for 5 min. Then, using immunohistochemical methods, the lower medulla of each rat was studied for NKA-, SP- and CGRP-IRs. Light microscopic examination of brain-stem sequencial sections revealed a simultaneous decrease in the immunoreactivities of all neuropeptides (NKA, SP and CGRP) in the CTN ipsilateral to TG stimulation in comparison with the other (not stimulated) side CTN. It is suggested that this decrease in immunoreactivity would be due to the co-release of neuropeptides following noxious stimuli and that NKA, SP and CGRP might therefore act as co-transmitters or co-modulators at the first central synapses of the trigeminal sensory pathway.

Alterations in neurokinin A-, substance P- and calcitonin gene-related peptide immunoreactivities in the caudal trigeminal nucleus of the rat following electrical stimulation of the trigeminal ganglion.

We have carried out an immunohistochemical study on the presence of neurokinin A (NKA) and substance P (SP) in the rat caudal trigeminal nucleus (CTN) after electrical stimulation of the trigeminal ganglion (TG), used as an experimental model to induce alterations, some of which may occur during migraine attacks (release of vasoactive peptides from perivascular trigeminal axons and neurogenic inflammation). Both unilateral, 30 min electrical stimulation (5 Hz, 5 ms, 0.1-1 mA) of the TG and 5 min stimulation with a slight increase in the stimulating parameters (7.5 Hz, 5 ms, 1.4 mA) caused a significant depletion of the NKA and SP immunoreactivities (-IR) of the TG nerve central terminals in the ipsilateral CTN. Calcitonin gene-related peptide (CGRP)-IR of the ipsilateral CTN was also studied in the CTN using the increased stimulating parameters and a marked depletion of CGRP-IR was also observed following TG stimulation. Such depletion may be due to the release of neuropeptides from the trigeminal central terminals. These findings suggest that NKA, SP and CGRP could act as neurotransmitters at the first central synapses of the trigeminal nociceptive pathway to transmit the sensory stimuli to the higher brain centers.