排序方式: 共有46条查询结果,搜索用时 15 毫秒
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Amol A. Verma Tejasvi Hora Hae Young Jung Michael Fralick Sarah L. Malecki Lauren Lapointe-Shaw Adina Weinerman Terence Tang Janice L. Kwan Jessica J. Liu Shail Rawal Timothy C.Y. Chan Angela M. Cheung Laura C. Rosella Marzyeh Ghassemi Margaret Herridge Muhammad Mamdani Fahad Razak 《CMAJ》2021,193(23):E859
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Saeid Ghassemi Nasser Delangiz Behnam Asgari Lajayer Davood Saghafi Filippo Maggi 《农业工程》2021,41(2):120-129
Medicinal plants play important role in industrial production of medicines. Moreover, they consume without complicated processes around the world. They are considered as healthy cure without any harmful side effects at least among ordinary people. Cold stress is one the harmful abiotic stresses and constrains medicinal plants yielding geographically. Cold acclimation is a process that induces cold stress resistance in temperate plants. Various structural and morphological alterations are involved in this process. Also, enzymatic and non-enzymatic agents play role in cold acclimation. Cell membrane modification and compatible solutes accumulation and so many other changes occur through cold acclimation. Growing under different stressful conditions, medicinal plants synthesize different components such as metabolites. Moreover, ROS can be generated in plant cells under stressful conditions. The accumulation of bioactive components, biosynthesis of phytohormones, ion hemostasis, osmolyte (compatible solutes) accumulation and changes in nutrient uptake, root system modification and systemic resistance are some of new investigations that are considered in this review. 相似文献
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Androutsellis-Theotokis A Ghassemi F Rudnick G 《The Journal of biological chemistry》2001,276(49):45933-45938
Serotonin transporter (SERT) contains a single reactive external cysteine residue at position 109 (Chen, J. G., Liu-Chen, S., and Rudnick, G. (1997) Biochemistry 36, 1479-1486) and seven predicted cytoplasmic cysteines. A mutant of rat SERT (X8C) in which those eight cysteine residues were replaced by other amino acids retained approximately 32% of wild type transport activity and approximately 56% of wild type binding activity. In contrast to wild-type SERT or the C109A mutant, X8C was resistant to inhibition of high affinity cocaine analog binding by the cysteine reagent 2-(aminoethyl)methanethiosulfonate hydrobromide (MTSEA) in membrane preparations from transfected cells. Each predicted cytoplasmic cysteine residue was reintroduced, one at a time, into the X8C template. Reintroduction of Cys-357, located in the third intracellular loop, restored MTSEA sensitivity similar to that of C109A. Replacement of only Cys-109 and Cys-357 was sufficient to prevent MTSEA sensitivity. Thus, Cys-357 was the sole cytoplasmic determinant of MTSEA sensitivity in SERT. Both serotonin and cocaine protected SERT from inactivation by MTSEA at Cys-357. This protection was apparently mediated through a conformational change following ligand binding. Although both ligands bind in the absence of Na(+) and at 4 degrees C, their ability to protect Cys-357 required Na(+) and was prevented at 4 degrees C. The accessibility of Cys-357 to MTSEA inactivation was increased by monovalent cations. The K(+) ion, which is believed to serve as a countertransport substrate for SERT, was the most effective ion for increasing Cys-357 reactivity. 相似文献
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AhmadAli Pourbabaee Amaneh Soleymani Ehssan Torabi Hassan Alizadeh 《Soil & Sediment Contamination》2018,27(8):756-772
ABSTRACTThe dissipation and detoxification of nicosulfuron (NS) by Pseudomonas aeruginosa B9 isolated from a cornfield soil was investigated. The fastest decline of NS occurred at 40 µg ml?1 in liquid media with 0.25% glucose plus 0.05% yeast extract (DT50 = 4 days) with a notable pH reduction (pH ? 5). Bioassay tests showed considerable phytotoxicity of NS for Cress (Lepidium sativum L.) with 50% shoot growth inhibition (SGI) at 40 µg ml?1. The dissipation of NS (40 µg ml?1) by the B9 isolate reduced the SGI significantly (SGI: up to 45 ± 3%) compared to the non-inoculated media (SGI: up to 58 ± 4%). In soils with the B9 isolate, NS dissipation, especially at 0.3 µg g?1, was faster with a more significant SGI reduction (k = 0.08 ± 0.00 day?1; SGI = 2 ± 1%) compared to non-inoculated samples (k = 0.03 ± 0.00 day?1; SGI = 8 ± 1%). NS initially inhibited soil respiration, microbial biomass carbon, and dehydrogenase activity. The effect was however transient, and these parameters recovered within 10 days, especially in the presence of the isolate. Overall, this study proves Pseudomonas aeruginosa B9 as a suitable candidate for bioremediation of NS in contaminated sites. 相似文献
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A recessive ryanodine receptor 1 mutation in a CCD patient increases channel activity 总被引:1,自引:0,他引:1
Farshid Ghassemi Mirko Vukcevic Le Xu Haiyan Zhou Gerhard Meissner Francesco Muntoni Heinz Jungbluth Francesco Zorzato Susan Treves 《Cell calcium》2009,45(2):192-197
Ryanodine receptors plays a crucial role in skeletal muscle excitation–contraction coupling by releasing calcium ions required for muscle contraction from the sarcoplasmic reticulum. At least three phenotypes associated with more than 100 RYR1 mutations have been identified; in order to elucidate possible pathophysiological mechanisms of RYR1 mutations linked to neuromuscular disorders, it is essential to define the mutation class by studying the functional properties of channels harbouring clinically relevant amino acid substitutions. In the present report we investigated the functional effects of the c.7304G > T RYR1 substitution (p.Arg2435Leu) found in a patient affected by central core disease. Both parents were heterozygous for the substitution while the proband was homozygous. We characterized Ca2+ homeostasis in myoD transduced myotubes from controls, the heterozygous parents and the homozygous proband expressing the endogenous mutation. We also expressed the recombinant mutant channels in heterologous cells and characterized their [3H]ryanodine binding and single channel properties. Our results show that the p.Arg2435Leu substitution affects neither the resting [Ca2+], nor the sensitivity of the ryanodine receptor to pharmacological activators, but rather reduces the release of Ca2+ from intracellular stores induced by pharmacological activators as well as by KCl via the voltage sensing dihydropyridine receptor. 相似文献
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Thomas J Epshtein Y Chopra A Ordog B Ghassemi M Christman JW Nattel S Cook JL Levitan I 《Journal of immunology (Baltimore, Md. : 1950)》2011,186(9):5236-5243
Anthrax lethal toxin (LeTx) is a virulence factor of Bacilillus anthracis that is a bivalent toxin, containing lethal factor (LF) and protective Ag proteins, which causes cytotoxicity and altered macrophage function. LeTx exposure results in early K(+) efflux from macrophages associated with caspase-1 activation and increased IL-1β release. The mechanism of this toxin-induced K(+) efflux is unknown. The goals of the current study were to determine whether LeTx-induced K(+) efflux from macrophages is mediated by toxin effects on specific K(+) channels and whether altered K(+)-channel activity is involved in LeTx-induced IL-1β release. Exposure of macrophages to LeTx induced a significant increase in the activities of two types of K(+) channels that have been identified in mouse macrophages: Ba(2+)-sensitive inwardly rectifying K(+) (Kir) channels and 4-aminopyridine-sensitive outwardly rectifying voltage-gated K(+) (Kv) channels. LeTx enhancement of both Kir and Kv required the proteolytic activity of LF, because exposure of macrophages to a mutant LF-protein (LF(E687C)) combined with protective Ag protein had no effect on the currents. Furthermore, blocking Kir and Kv channels significantly decreased LeTx-induced release of IL-1β. In addition, retroviral transduction of macrophages with wild-type Kir enhanced LeTx-induced release of IL-1β, whereas transduction of dominant-negative Kir blocked LeTx-induced release of IL-1β. Activation of caspase-1 was not required for LeTx-induced activation of either of the K(+) channels. These data indicate that a major mechanism through which LeTx stimulates macrophages to release IL-1β involves an LF-protease effect that enhances Kir and Kv channel function during toxin stimulation. 相似文献
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Andrea C. Tricco Jesmin Antony Noah M. Ivers Huda M. Ashoor Paul A. Khan Erik Blondal Marco Ghassemi Heather MacDonald Maggie H. Chen Lianne Kark Ezer Sharon E. Straus 《CMAJ》2014,186(15):E568-E578