Galvanizing for the future: a bottom-up departmental approach to diversity, equity, and inclusion.

As an academic department, we sought to identify effective strategies to engage our faculty and staff in diversity, equity, and inclusion initiatives and programs to build an inclusive department that would address our needs and those of our community and partners. Over a 4-year period, our faculty and staff have participated in town hall meetings, focus group discussions, surveys, and community-building activities to foster stakeholder engagement that will build a leading academic department for the future. We noted that our faculty and staff were committed to building diversity, equity, and inclusion, and our mission and vision were reflective of this. However, communication and transparency may be improved to help support a more inclusive department for all. In the future, we hope to continue with the integration of diversity, equity, and inclusion into our department's business processes to achieve meaningful, sustained change and impact through continued focus on recruitment, selection, retention, development, and wellness of faculty and staff-in addition to the continued recruitment of faculty and staff from underrepresented minority groups. Our findings should serve as a call to action for other academic obstetrics and gynecology departments to improve the health and well-being of the individuals we serve.

[Effect of gangliosides on intensity of the lipid peroxidation process and structural changes in neuronal membranes, caused by toxic doses of glutamate]. / Vliianie gangliozidov na intensivnost' protsessov perekisnogo okisleniia lipidov i strukturnye izmeneniia neironal'noi membrany, vyzvannye toksicheskimi dozami glutamata.

We studied effects of gangliosides on the level of lipid peroxides and microviscosity of membrane lipid bilayer in primary dissociated cultures of cerebellar granule cells prepared from 8 day-old rats under conditions of neurotoxic effect of glutamate. It was found that glutamate (100 mkM) treatment of primary cultures activated the processes of lipid peroxidation and decreased microviscosity of neuronal membranes determined as a degree of pyrene excimerization. It was also shown that preincubation of granule cells with gangliosides did not prevent the accumulation of TBA-reactive products induced by glutamate. At the same time gangliosides significantly decreased the membrane-fluidizing effect caused by glutamate.

Hypoxic and posthypoxic neuronal injury in hippocampal cell culture: attenuation by lipophylic antioxidant U-18 and superoxide dismutase.

The neuroprotective effects of synthesized lipophylic antioxidant from hindered phenol class (U-18) and hydrophylic antioxidative enzyme superoxide dismutase (SOD) were tested on long-term mouse hippocampal cell cultures exposed to hypoxia/reoxygenation. The application of U-18 to the cultures during 6-8 hr hypoxia followed by 16-18 hr reoxygenation in the absence of antioxidant significantly reduced neuronal death. Thus, lipophylic free radical scavenger may exert a delayed neuroprotective effect, probably owing to persistent incorporation into phospholipid membranes and prevention of their lipid peroxidation by means of prolonged intramembranous free radical quenching. On the other hand, the exposure of the cultures to U-18 during 15 hr hypoxia without subsequent reoxygenation also led to significant reduction of neuronal death compared with that observed without antioxidant. These findings suggest that free radical neuronal damage may occur under conditions of prolonged restricted oxygen access to the neurons. The hypoxic/posthypoxic neuronal injury significantly decreased in the cultures exposed to hydrophylic cytoplasmic enzyme SOD (300 U/ml). The neuroprotective effects of both lipophylic U-18 and hydrophylic SOD on the cultures exposed to hypoxia/reoxygenation might reflect the damaging free radical overproduction in different morphofunctional compartments of the nerve cell.

[Ganglioside participation in the regulation of free-radical reactions in brain membranes]. / Uchastie gangliozidov v reguliatsii svobodnoradikal'nykh reaktsii v membranakh mozga.

The effect of monosialoganglioside GM1 on induced free radical reactions in the synaptosomal and myelin membranes induced by Fe(2+)-H2O2 system was studied. The formation of free radicals was determined by measuring luminol-dependent chemoluminescence. It was found that preincubation of the membranes with GM1 (10(-11)-10(-6) M) and 12 or 12-palmitate, 13-acetate phorbol ester (10(-7)-10(-6) M) or alpha-tocopherol (10(-6) M) results in the decrease of chemiluminescent response. The inhibiting effect of alpha-tocopherol (but not of other compound tested) takes place without any preincubation as well. When the effect of GM1 was studied over a wide range of GM1 concentrations, a biphasic kinetics was observed, the highest per cent of inhibition of chemoluminescence being found at 10(-8) M. The data obtained provide evidence that the inhibition of free radical reactions in the brain membranes by nanomolar concentration of GM1 is not due to its interaction with lipid radicals. The results suggested that the inhibiting effect of GM1 is mediated through signal transduction system.

[Protection of cultured hippocampal neurons in hypoxia and subsequent reoxygenation by antioxidant from the spatially hindered phenols class]. / Zashchita kul'tiviruemykh neironov gippokampa pri gipoksii i posleduiushchei reoksigenatsii antioksidantom klassa prostranstvenno-zatrudnennykh fenolov.

The influence of antioxidant from hindered phenols (U-18) on a hypoxic neurodestructive effect in mouse hippocampal cell cultures was studied. Morphological and biochemical quantitative analysis of neuronal damage showed that U-18 attenuates nerve cell death resultant from 6-7-hour hypoxia and subsequent 12-hour posthypoxic reoxygenation. This antidestructive action of U-18 was observed upon its introduction in nutrient medium both before and immediately after hypoxic period. Thus, our results suggest that peroxidant reactions play a pivotal role in hypoxic neuronal injury and probably participate in this neurodestructive process mainly during posthypoxic reoxygenation period.

[Effects of nitroxyl radicals on pathogenic properties of herpesvirus (the spin-label technique in the study of virus-macrophage interactions)]. / Vliianie nitroksil'nykh radikalov na patogennye svoistva virusa Gerpesa (metod spinovogo zondirovaniia v issledovanii vzaimodeistviia virus-makrofag).

The effect of various concentrations of both methyl ether of 5-doxyl-stearic acid (M5DS) and 4-maleimido-TEMPO (4MT) on the pathogenicity of herpes simplex virus (HSV-1) was studied. It is known that the reagents modify the lipid matrix and the proteins of virion envelope. The decrease of the HSV-1 pathogenicity was shown when using the concentration of reagents more 5 x 10(-5) M. HSV-1 having high pathogenicity and cytotoxicity was obtained when the concentrations of the reagents were less 5 x 10(-5) M.

[Protection of beta-adrenoreceptors of the rat brain during emotional-pain stress by oxidants of the steric hindrance class of phenols]. / Zashchita beta-adrenoretseptorov mozga krys pri émotsional'no-bolevom stresse antioksidantom klassa prostranstvenno-zatrudnennykh fenolov.

Adaptogenic properties of a new antioxidant-isoquinoline derivative of hindered phenol class under pain-emotional stress have been investigated. This new antioxidant was shown to have stress-protective effects, i.e. it stabilizes cerebral beta-adrenoreceptors, inhibits lipid peroxidation and stimulates anti-radical defense systems in the brain and serum, as well as normalizes vegetative functions in rats.

[Alpha-tocopherol protects beta-adrenoreceptors of the rat brain from damaging effects of phospholipase A2]. / alfa-tokoferol zashchishchaet beta-adrenoretseptory mozga krys ot povrezhdaiushchego deistviia fosfolipazy A2.

The effect of synaptosomal membrane phospholipid hydrolysis by phospholipase A2 and alpha-tocopherol upon the state of beta-adrenergic receptors has been studied. The damaging action of phospholipase A2 on beta-adrenergic receptors, consisting in the decrease of specific binding of 3H-dihydroalprenolol at the expense of diminishing receptor affinity and Bmax was demonstrated. It was shown, that alpha-tocopherol protects beta-adrenergic receptors from damaging effect of phospholipase A2.

[Role of isoprenoid chain of lateral mobility of alpha-tocopherol in lipid bilayer]. / Rol' izoprenoidnoi tsepi lateral'noi podvizhnosti alfa-tokoferola v lipidnom bisloe.

Using the quenching effect of the fluorescence by nitroxyl radicals the lateral mobility of chromanols in the lipid bilayer was studied. The lateral mobility of the chromanols was shown to increase when the length of phytol chain was diminished. The result is consistent with the idea that antioxidant affect of the chromanols depends on their lateral mobility.

[Luminol and lucigenin-dependent chemiluminescence in 6-hydroxydopamine auto-oxidation]. / Liuminol- i liutsigeninzavisimaia khemliuminestsentsiia pri avtookislenii 6-oksidofamina.

It was shown by the methods of luminol- and lucigenin-dependent chemiluminescence that 6-hydroxydopamine 6-ONDA autooxidation is accompanied by generation of superoxide anion-radical which can further react with next 6-ONDA molecule. This fact is based on the observations that intensities of luminol- and lucigenin-dependent chemiluminescence during 6-ONDA autooxidation was increased in aprotonic aqueous solutions (with the decreasing of pH) and was extremely depended on 6-ONDA concentration. The obtained data allows to suggest that one of the possible mechanisms of 6-ONDA neurotoxic action includes the generation of superoxide, whose dismutation to hydrogen peroxide in the presence of transient valency ions gives rise to HO.

[Participation of gangliosides in protection of beta adrenergic receptors from damaging effect induced by lipid peroxidation in synaptosome membranes]. / Uchastie gangliozidov v zashchite beta-adrenoretseptorov ot povrezhdaiushchego vozdeistviia, vyzvannogo perekisnym okisleniem lipidov, v membranakh sinaptosom.

The induction of lipid peroxidation (LPO) in rat brain synaptosomes was shown to result in considerable decrease of the level of specific [3H]-dihydroalprenolol binding, decrease of Bmax and increase of KD. It was revealed that the preincubation of rat brain synaptosomes with monosialoganglioside GM1 (10(-8) M) or alpha-tocopherol (10(-6) M) led to a decrease in MDA accumulation after LPO induction by Fe(2+)-ascorbate system. AT the same time GM1 prevents damage of beta-adrenoreceptors, caused by LPO induction, having no effect on the functional state of beta-adrenoreceptors in control preparations. Partial normalization of the ligand affinity of the receptors was observed after preincubation of synaptosomes with GM1 and alpha-tocopherol. The various mechanisms of stabilization of synaptosomal membranes by gangliosides and natural antioxidant-tocopherol is suggested.

[Mechanism of antioxidant action of carnosine]. / Mekhanizm antioksidantnogo deistviia karnozina.

The comparative study of the antiradical activity of carnosine and vitamin C was carried out by the means of the evaluation of quenching of ESR signals of 2,2-diphenyl-1-picrylhydrazyl (DFPH) and semiquinone radical of alpha-tocopherol. It was shown that carnosine is not able to quench the ESR signals of the stable radical of DFPH and semiquinone radical of alpha-tocopherol. It permits to conclude that: a) carnosine does not interact directly with highly active free radicals; b) carnosine is unable to regenerate the radical of alpha-tocopherol to form the antiradical synergistic couple. The data obtained are consistent with the idea that there is a difference between on the antioxidant mechanism action of vitamin C and carnosine due to the difference in the antiradical activity of these compounds.

[Vitamin E decreases the neurocytotoxic action of kainic acid in a cerebellar neuron culture]. / Vitamin E snizhaet neirotsitotoksicheskoe deistvie kainovoi kisloty v kul'ture neironov mozzhechka.

Using primary cultures of cerebellar granule cells from 4-6-day old Wistar rats we showed the protective effect of vitamin E against kainate-induced neurotoxicity. The preincubation of 7-8-day old cultures with 5 x 10(-4) M alpha-tocopherol solution significantly (on 10-20%) reduces the number of damaged granule cells. As vitamin E takes part in stabilization of membrane lipids the data presented allows us to suggest that one of the possible mechanisms of neuronal injury includes lipid oxidation of the neuronal membranes which leads to additional influx of Ca2+ and results in neuronal death.

Mechanisms of stabilization of biomembranes by alpha-tocopherol. The role of the hydrocarbon chain in the inhibition of lipid peroxidation.

The effects of alpha-tocopherol and its homologues with different chain lengths (6-hydroxy-chromanes: C1, C6, C11) on lipid peroxidation in natural membranes (liver microsomes and mitochondria, brain synaptosomes) and liposomes were studied. It was shown that the antioxidant activity of alpha-tocopherol homologues decreased in the order: C1 greater than C6 greater than C11 greater than alpha-tocopherol (C16). Using fluorescent measurements, the possible reasons underlying these differences were investigated: (i) the distribution between the aqueous media and nonpolar phase of the membrane, which predetermines the binding of alpha-tocopherol homologues to membranes; (ii) the incorporation of alpha-tocopherol homologues into lipid bilayer; (iii) non-uniform distribution (formation of the clusters) of tocopherol homologues in the lipid bilayer; and (iv) transbilayer mobility of alpha-tocopherol homologues and accessibility of the inhibitors for radical-generating centres under enzymically and non-enzymically induced lipid peroxidation. It was demonstrated that: (i) binding of C1 with membranes was less efficient than that of longer-chain homologues (C6, C11, C16); (ii) the level of incorporation of alpha-tocopherol homologues into membranes decreased in a succession alpha-tocopherol C11 greater than C6 greater than C1; (iii) all alpha-tocopherol homologues existed in the lipid bilayer not only in a monomeric form but also associated in clusters thus decreasing the efficiency of radical scavenging; (iv) the short-chain alpha-tocopherol homologue, C1, exhibited a high transbilayer mobility whereas the long-chain one, C16, underwent no transbilayer migration within tens of minutes. The inhibiting effect of alpha-tocopherol esters and C1-acetate was predetermined by their hydrolysis in biomembranes; a strong correlation exists between the rate of the ester hydrolysis and their antioxidant activity in the membrane. In liposomes, in which the esterase activity was absent, alpha-tocopherol esters and C1-acetate exhibited very low lipid peroxidation inhibition.