430 research outputs found

    Магнитокоммутируемая микросхема и датчик измерения скорости ветра на ее основе

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    Разработанная магнитокоммутируемая микросхема на основе эффекта Холла позволила создать магнитный датчик скорости ветра.У статті представлено опис магн·токомутуємої мікросхе·ми на основі ефекту Холу. Приведені електрична схема розробленої МКМ і її основні технічні характеристики. Розроблено датчик швидкості вітру на її основі. Діапазон вимірювання швидкості вітру склав 0,5 - 50 м/с з похибкою ±5%.The magneto switch microcircuit on the base of Hall-effect is developed. The electric scheme of the magneto sensitive IC was designed and its basic technical characteristics are described. The gauge of wind speed on its base is fabricated

    A ligand for the aryl hydrocarbon receptor isolated from lung

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    Author Posting. © National Academy of Sciences, 2002. This article is posted here by permission of National Academy of Sciences for personal use, not for redistribution. The definitive version was published in Proceedings of the National Academy of Sciences 99 (2002): 14694-14699, doi:10.1073/pnas.232562899.The aryl hydrocarbon receptor (AHR) is a ligand-inducible transcription factor that is best known because it mediates the actions of polycyclic and halogenated aromatic hydrocarbon environmental toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin. We report here the successful identification of an endogenous ligand for this receptor; {approx}20 µg was isolated in pure form from 35 kg of porcine lung. Its structure was deduced as 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester from extensive physical measurements and quantum mechanical calculations. In a reporter gene assay, this ligand activates the AHR with a potency five times greater than that of {beta}-naphthoflavone, a prototypical synthetic AHR ligand. 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester competes with 2,3,7,8-[3H]tetrachlorodibenzo-p-dioxin for binding to human, murine, and fish AHRs, thus showing that AHR activation is caused by direct receptor binding, and that recognition of this endogenous ligand is conserved from early vertebrates (fish) to humans.This work was supported by the Wisconsin Alumni Research Foundation, the University of Wisconsin Sea Grant Institute, and the National Institutes of Health

    Вплив екологічного стану Донецького регіону на його демографічний розвиток

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    В статті розглянуто важливу проблему впливу забрудненості навколишнього природного середовища на захворюваність та смертність в регіоні. Визначено кореляційну залежність між обсягом викидів забруднюючих речовин та окремими видами захворюваності, а також ступінь їх впливу, побудовано функції, що описують їх.В статье рассмотрена важная проблема влияния загрязненности окружающей естественной среды на заболеваемость и смертность в регионе. Определена корреляционная зависимость между объемом выбросов загрязняющих веществ и отдельными видами заболеваемости, а также степень их влияния, построены функции, которые описывают их.In the article the important problem of influence of muddiness of natural environment is considered on morbidity and death rate in a region. Certainly cross-correlation dependence between the volume of extrass of contaminents and separate types of morbidity, and also degree of their influence, functions which describe them are built. Keywords: environment

    Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A

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    INTRODUCTION: This study was designed to determine if and how a non-toxic, naturally occurring bioflavonoid, galangin, affects proliferation of human mammary tumor cells. Our previous studies demonstrated that, in other cell types, galangin is a potent inhibitor of the aryl hydrocarbon receptor (AhR), an environmental carcinogen-responsive transcription factor implicated in mammary tumor initiation and growth control. Because some current breast cancer therapeutics are ineffective in estrogen receptor (ER) negative tumors and since the AhR may be involved in breast cancer proliferation, the effects of galangin on the proliferation of an ER(-), AhR(high )line, Hs578T, were studied. METHODS: AhR expression and function in the presence or absence of galangin, a second AhR inhibitor, α-naphthoflavone (α-NF), an AhR agonist, indole-3-carbinol, and a transfected AhR repressor-encoding plasmid (FhAhRR) were studied in Hs578T cells by western blotting for nuclear (for instance, constitutively activated) AhR and by transfection of an AhR-driven reporter construct, pGudLuc. The effects of these agents on cell proliferation were studied by (3)H-thymidine incorporation and by flow cytometry. The effects on cyclins implicated in mammary tumorigenesis were evaluated by western blotting. RESULTS: Hs578T cells were shown to express high levels of constitutively active AhR. Constitutive and environmental chemical-induced AhR activity was profoundly suppressed by galangin as was cell proliferation. However, the failure of α-NF or FhAhRR transfection to block proliferation indicated that galangin-mediated AhR inhibition was either insufficient or unrelated to its ability to significantly block cell proliferation at therapeutically relevant doses (IC(50 )= 11 μM). Galangin inhibited transition of cells from the G(0)/G(1 )to the S phases of cell growth, likely through the nearly total elimination of cyclin D3. Expression of cyclins A and E was also suppressed. CONCLUSION: Galangin is a strong inhibitor of Hs578T cell proliferation that likely mediates this effect through a relatively unique mechanism, suppression of cyclin D3, and not through the AhR. The results suggest that this non-toxic bioflavonoid may be useful as a chemotherapeutic, particularly in combination with agents that target other components of the tumor cell cycle and in situations where estrogen receptor-specific therapeutics are ineffective

    Assessment of phenolic herbicide toxicity and mode of action by different assays

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    A phytotoxicity assay based on seed germination/root elongation has been optimized and used to evaluate the toxic effects of some phenolic herbicides. The method has been improved by investigating the influence of experimental conditions. Lepidium sativum was chosen as the most suitable species, showing high germinability, good repeatability of root length measurements, and low sensitivity to seed pretreatment. DMSO was the most appropriate solvent carrier for less water-soluble compounds. Three dinitrophenols and three hydroxybenzonitriles were tested: dinoterb, DNOC, 2,4-dinitrophenol, chloroxynil, bromoxynil, and ioxynil. Toxicity was also determined using the Vibrio fischeri MicrotoxA (R) test, and a highly significant correlation was found between EC50 values obtained by the two assays. Dinoterb was the most toxic compound. The toxicity of hydroxybenzonitriles followed the order: ioxynil > bromoxynil > chloroxynil; L. sativum exhibited a slightly higher sensitivity than V. fischeri to these compounds. A QSAR analysis highlighted the importance of hydrophobic, electronic, and hydrogen-bonding interactions, in accordance with a mechanism of toxic action based on protonophoric uncoupling of oxidative phosphorylation. The results suggest that the seed germination/root elongation assay with L. sativum is a valid tool for the assessment of xenobiotic toxicity and can be recommended as part of a test battery
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