[THE REGULARITIES OF DEVELOPMENT OF CANCER MORBIDITY AND MORTALITY RATE OF THE POPULATION IN THE REPUBLIC OF TATARSTAN AND FINLAND].

There were revealed gender differences in cancer morbidity and mortality rate in the Republic of Tatarstan over the period from 1996 till 2013. The morbidity rate was increased by 1.54 times in both urban and rural areas. The morbidity rate level in men was two times higher than in women. The maximum share of new cases of cancer morbidity according to the primary lesion in men in Finland in 2008-2012 was noted in the age groups of 60-64, 70-79 and 85 years and older

[THE REGULARITIES OF DEVELOPMENT OF CANCER MORBIDITY AND MORTALITY RATE OF THE POPULATION IN THE REPUBLIC OF TATARSTAN AND FINLAND].

There were revealed gender differences in cancer morbidity and mortality rate in the Republic of Tatarstan over the period from 1996 till 2013. The morbidity rate was increased by 1.54 times in both urban and rural areas. The morbidity rate level in men was two times higher than in women. The maximum share of new cases of cancer morbidity according to the primary lesion in men in Finland in 2008-2012 was noted in the age groups of 60-64, 70-79 and 85 years and older.

Cortical spreading depression induces oxidative stress in the trigeminal nociceptive system.

Indirect evidence suggests the increased production of reactive oxygen species (ROS) in migraine pathophysiology. In the current study we measured lipid peroxidation product in the rat cortex, trigeminal ganglia and meninges after the induction of cortical spreading depression (CSD), a phenomenon known to be associated with migraine aura, and tested nociceptive firing triggered by ROS in trigeminal nerves ex vivo. Application of KCl to dura mater in anesthetized rats induced several waves of CSD recorded by an extracellular electrode in the cortex. Following CSD, samples of cortex (affected regions were identified with blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI)), meninges from left and right hemispheres and trigeminal ganglia were taken for biochemical analysis. We found that CSD increased the level of the lipid peroxidation product malondialdehyde (MDA) in the ipsilateral cerebral cortex and meninges, but also in both ipsi- and contralateral trigeminal ganglia. In order to test the pro-nociceptive action of ROS, we applied the mild oxidant hydrogen peroxide to isolated rat hemiskull preparations including preserved trigeminal innervations. Application of hydrogen peroxide to meninges transiently enhanced electrical spiking activity of trigeminal nerves showing a pro-nociceptive action of ROS. In the presence of hydrogen peroxide trigeminal nerves still responded to capsaicin by burst of spiking activity indicating integrity of neuronal structures. The action of hydrogen peroxide was mediated by TRPA1 receptors as it was abolished by the specific TRPA1 antagonist TCS-5861528. Using dorsal root ganglion sensory neurons as test system we found that hydrogen peroxide promoted the release of the migraine mediator calcitonin gene-related peptide (CGRP), which we previously identified as a trigger of delayed sensitization of trigeminal neurons. Our data suggest that, after CSD, oxidative stress spreads downstream within the trigeminal nociceptive system and could be involved in the coupling of CSD with the activation of trigeminovascular system in migraine pathology.