Fetus sound stimulation: cilia memristor effect of signal transduction.

BACKGROUND: This experimental study evaluates fetal middle cerebral artery (MCA) circulation after the defined prenatal acoustical stimulation (PAS) and the role of cilia in hearing and memory and could explain signal transduction and memory according to cilia optical-acoustical properties. METHODS: PAS was performed twice on 119 no-risk term pregnancies. We analyzed fetal MCA circulation before, after first and second PAS. RESULTS: Analysis of the Pulsatility index basic (PIB) and before PAS and Pulsatility index reactive after the first PAS (PIR 1) shows high statistical difference, representing high influence on the brain circulation. Analysis of PIB and Pulsatility index reactive after the second PAS (PIR 2) shows no statistical difference. Cilia as nanoscale structure possess magnetic flux linkage that depends on the amount of charge that has passed between two-terminal variable resistors of cilia. Microtubule resistance, as a function of the current through and voltage across the structure, leads to appearance of cilia memory with the "memristor" property. CONCLUSION: Acoustical and optical cilia properties play crucial role in hearing and memory processes. We suggest that fetuses are getting used to sound, developing a kind of memory patterns, considering acoustical and electromagnetically waves and involving cilia and microtubules and try to explain signal transduction.

[Comparison of two different types of hormone therapy effects on haemostatic parameters in early postmenopausal women].

INTRODUCTION: Most postmenopausal women have some of menopausal symptoms due to oestrogen deprivation. Many therapeutic options are available for managing menopausal problems. However, hormone therapy is associated with a heightened risk for thromboembolic events. OBJECTIVE: To investigate the effects of different types of hormone therapy on some haemostatic parameters. METHODS: This randomized, controlled study included 56 healthy, early postmenopausal women aged 46-58 years on different types of hormone therapy (tibolone 2.5 mg/day, 25 women, or CCHT 2 mg estradiol plus 1 mg norethisteron acetate, 31 women) and 20 healthy postmenopausal women of the same age receiving placebo. Effects of these 2 medicaments on some haemostasis parameters were measured 3 and 6 months after the onset of treatment. RESULTS: Short-term use (3 months) of both tibolone and CCHT had a detrimental effect on antithrombin, protein C and protein S levels (decreased), and even more so in the group treated with CCHT. Plasminogen-activator inhibitor type 1 levels were decreased by both tibolone and CCHT, but more so by CCHT; thrombin-antithrombin complex were increased in both groups. There were no changes in haemostatic parameters between 3-month and 6-month treatment in any group. CONCLUSION: Both therapeutic options are associated with an activation of thrombogenic and fibrinolytic markers within 3 months of use. Tibolone appears to produce a better balance between thrombogenesis and fibrinolysis. Since our results show a lower incidence of thrombotic events, further studies are required.

[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome].

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.