Original scientific article describes female sex behavior and hypothalamic expression of progesterone receptor in SF-1 knockout mice. It was established that sex differences in both, expression of female sex behavior and immunoexpression of progesterone receptor in the hypothalamus are likely partially dependent on genes from sex chromosomes as sex specific differences were found also between male and female SF-1 KO mice that have never been exposed to sex steroid hormones. The manuscript has already been cited three times in one year since publication.
COBISS.SI-ID: 3520890
The aim of this retrospective study was to determine significant differences of selected parameters between groups, according to the IFA titres (6 groups) and PCR positive result (one group) in attempt to improve current diagnostic and treatment criteria. Thrombocytopenia was the most prominent change in all positive dogs. There were significant differences only between each positive group compared to the control group. Our results showed the necessity of introducing additional diagnostic procedures in clinical practice to confirm the clinical relevance of exposure to A. phagocytophilum. Article has been cited four times since publication.
COBISS.SI-ID: 28169945
Original scientific article on the effect of social isolation on social behavior in laboratory mice. The article is especially important from two perspectives. Firstly, it shows that breeding conditions have profound effects on behavior in laboratory mice and must therefore be taken into account when performing behavioral analyzes. Secondly, it shows that even transient social isolation has long lasting effects on mouse behavior, most likely achieved through epigenetic mechanisms, and this could have important implications also for human mental health. Article has been cited eight times since publication.
COBISS.SI-ID: 3261050
APS12-2, a non-competitive acetylcholinesterase inhibitor, is one of the synthetic analogues of polymeric alkylpyridinium salts (poly-APS) isolated from the marine sponge Reniera sarai. It is a non-competitive acetylcholinesterase inhibitor. In the present work the effects of APS12-2 were studied on isolated mouse phrenic nerve-hemidiaphragm muscle preparations, using twitch tension measurements and electrophysiological recordings. APS12-2 in a concentration-dependent manner blocked nerve-evoked isometric muscle contraction (IC50 = 0.74 µM), without affecting directly-elicited twitch tension up to 2.72 µM. We studied the influence of APS12-2 on endplate potentials in mouse diaphragm muscle fibers using intracellular microelectrode technique. The compound (0.007–3.40 µM) decreased the amplitude of miniature endplate potentials until a complete block by concentrations higher than 0.68 µM, without affecting their frequency. Full size endplate potentials, recorded after blocking voltage-gated muscle sodium channels, were inhibited by APS12-2 in a concentration-dependent manner (IC50 = 0.36 µM) without significant change in the resting membrane potential of the muscle fibers up to 3.40 µM. The compound also blocked acetylcholine-evoked inward currents in Xenopus oocytes in which Torpedo (α12β1γδ) muscle-type nicotinic acetylcholine receptors (nAChRs) have been incorporated (IC50 = 0.0005 µM) indicating a higher affinity of the compound for Torpedo (α12β1γδ) than for the mouse (α12β1γε) nAChR. Our data show for the first time that APS12-2 blocks neuromuscular transmission by a non-depolarizing mechanism through an action on postsynaptic nAChRs of the skeletal neuromuscular junction. This article was recognised as an oustanding scintific achivement in the field of biotechnical sciences for 2012.
COBISS.SI-ID: 3587706
During high intensity exercise approximately 4% of the cardiac output leaves the pulmonary circulation into the interstitium. This fluid flux has been thought to originate from plasma and attributed to an increase in pulmonary transmural hydrostatic (Starling) forces, increases in perfused microvascular surface area and reversible alterations in capillary permeability. However, fluid efflux from erythrocytes may account for a considerable fraction of fluid exiting the pulmonary circulation. Transcapillary erythrocyte volume changes are largely determined by the Jacobs-Stewart cycle, which determines CO2 metabolism in systemic and pulmonary capillaries. We tested the hypothesis that the Jacobs-Stewart cycle contributes to pulmonary transvascular fluid fluxes during exercise by inhibiting red cell carbonic anhydrase, whose activity is critical to rapid completion of the Jacobs-Stewart cycle during capillary transit. Carbonic anhydrase inhibition was achieved with treatment with acetazoamide. The results indicate that during exercise in horses, transvascular fluid fluxes in the lung appear to be dependent on the Jacobs-Stewart cycle and much less dependent upon transmural hydrostatic (Starling) forces.
COBISS.SI-ID: 3698810