The sustainability of the information lies in the system's guarantee that anelectronic record will be returned in an intelligible manner throughout its retentionperiod. Part of the documentary memory of our society created and preserved ondigital media is already compromised, and the costs of restoring electronic recordsare very high. In addition, the fragility of the media and technological obsolescencemust be addressed.

An enhanced vasoconstrictor activity of cutaneous arteries participates in the reduction of skin blood flow induced by cooling stimulation. Raynaud's phenomenon, which is characterized by intense cooling-induced constriction of cutaneous arteries, is more common in women during the period from menarche to menopause. We thus investigated the effect of 17β-estradiol (E2) on cooling-induced reduction of plantar skin blood flow (PSBF) in mouse in vivo. Ovariectomized female ddY mice, anaesthetized with pentobarbital, were treated with tetrodotoxin for eliminating the sympathetic nerve tone and artificially ventilated. The PSBF was measured by laser Doppler flowmetry. Cooling air temperature around the foot from 25 to 20, 15, or 10 °C decreased the PSBF in a temperature-dependent manner, which was suppressed by the specific α2C-adrenoceptor antagonist MK-912. When E2 was intravenously administered as a bolus followed by a constant infusion for 10 min just before the cooling stimulation, the cooling-induced reduction of PSBF was facilitated by E2 in a dose-dependent manner. The facilitatory effect of E2 was not induced after the treatment with MK-912. Similar facilitatory effect was induced by an intravenous application of G-1, an agonist of G protein-coupled estrogen receptor (GPER, also termed GPR30). Moreover, the facilitatory effect of E2 was abolished by the GPER antagonist G15. These results suggest that acute administration of E2 leads to the facilitation of cooling-induced, α2C-adrenoceptor-mediated reduction of skin blood flow via the activation of the non-genomic estrogen receptor GPER.

PD is a neurodegenerative disease characterized with loss of dopamine neurons and associated with neuroinflamation and unbalanced in HPA-axis. We investigated the content of cortisol and DEAS - hormones of HPA-axis in patients with PD after applying rTMS. Feng S.F. et al. (2012) showed that rTMS improves the balance of HPA axis hormones during depression, which is one of the non-motor manifestations of PD. PD patients were randomized into groups with active rTMS (13 men, 11 women) and sham rTMS (10 men, 15 women).The 10Hz rTMS was performed sequentially over 2 targets: the primary motor cortex and the DLPFC daily for 20 days. Outcome measures included the indicators of MDS-UPDRS (Part 3) scale, content of cоrtisol and DEAS in the peripheral blood.The Motor Examination Part scores demonstrated clinically meaningful improvement only in the active treatment group (p < 0.01). The content of the DEAS in this group was negatively correlated with indicators of scales of clinical manifestations, stress and anxiety (p < 0.05). In this group an increase of content of DEAS in the peripheral blood of men was found (p < 0.01, Wald-Wolfowitz Runs Test). Thus, the rTMS increases the levels of a wellknown neuroprotective hormone and a modulator of DA activity DEAS only in men.

We analyzed variability of the expression of three reference genes in biopsy samples of the olfactory epithelium obtained from healthy volunteers. The expression of B2M, HPRT1, and CASC3 genes was analyzed by real-time PCR. The pairs of genes B2M-HPRT1 and B2M-CASC3 were found to possess minimum individual variability of expression and can be reliable candidates for the reference genes in analysis of gene expression in neural cells.

The parallel placebo-controlled study examined the therapeutic effects of dual-target repetitive transcranial magnetic stimulation (rTMS) of the motor cortex (bilaterally) and the left prefrontal cortex (dorsolaterally) on spontaneous and mitogen-stimulating synthesis of pro- and anti-inflammatory cytokines by the blood cells and the level of brain-derived neurotrophic factor (BDNF) in blood serum of patients with Parkinson's disease. The significantly steeper positive clinical dynamics (assessed by UPRSD scale) observed in rTMS group in comparison with the placebo group was accompanied by a significant drop in spontaneous production of proinflammatory cytokines IFNγ and IL-17A. rTMS produced no significant effect on serum BDNF. The possible mechanisms of rTMS therapeutic action on the level of cytokines associated with neuroinflammation in patients with Parkinson's disease are discussed.

Introduction: The approach intended evaluating treatment potential of dual-target navigated rTMS in Parkinson's disease (PD) patients. We aimed at the M1 target for motor symptoms and at the left DLPFC for frequently co-occuring depression.