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81.
Suresh K. Gupta Vivekananthan Kalaiselvan Sushma Srivastava Rohit Saxena Shyam S. Agrawal 《Biological trace element research》2010,136(3):258-268
Cataract is the opacification in eye lens and leads to 50% of blindness worldwide. The present study was undertaken to evaluate
the anticataract potential of Trigonella foenum-graecum Linn seeds (fenugreek) in selenite-induced in vitro and in vivo cataract. In vitro enucleated rat lenses were maintained
in organ culture containing Dulbecco’s modified Eagles medium (DMEM) alone or in addition with 100 μM selenite and served
as the normal and control groups, respectively. For the test group, the medium was supplemented with selenite and T. foenum-graecum aqueous extract. The lenses were incubated for 24 h at 37°C. After incubation, the lenses were processed for the estimation
of reduced glutathione (GSH), lipid peroxidation product (malondialdehyde), and the antioxidant enzymes. In vivo selenite
cataract was induced in 9-day-old rats by subcutaneous injection of sodium selenite (25 μmol/kg body weight). Animals in the
test group were injected with different doses of aqueous extract of T. foenum-graecum 4 h before the selenite challenge. A fall in GSH and a rise in malondialdehyde levels were observed in control as compared
to normal lenses. T. foenum-graecum significantly (P < 0.01) restored glutathione and decreased malondialdehyde levels. A significant restoration in the activities of antioxidant
enzymes such as superoxide dismutase (P < 0.01), catalase, (P < 0.01), glutathione peroxidase (P < 0.01), and glutathione-S-transferase (P < 0.01) was observed in the T. foenum-graecum supplemented group as compared to control. In vivo, none of the eyes was found with nuclear cataract in treated group as
opposed to 72.5% in the control group. T. foenum-graecum protects against experimental cataract by virtue of its antioxidant properties. Further studies are warranted to explore
its role in human cataract. 相似文献
82.
A new flow-structure interaction method is presented, which couples a sharp-interface immersed boundary method flow solver with a finite-element method based solid dynamics solver. The coupled method provides robust and high-fidelity solution for complex flow-structure interaction (FSI) problems such as those involving three-dimensional flow and viscoelastic solids. The FSI solver is used to simulate flow-induced vibrations of the vocal folds during phonation. Both two- and three-dimensional models have been examined and qualitative, as well as quantitative comparisons, have been made with established results in order to validate the solver. The solver is used to study the onset of phonation in a two-dimensional laryngeal model and the dynamics of the glottal jet in a three-dimensional model and results from these studies are also presented. 相似文献
83.
Cholesterol and its hemisuccinate and sulfate derivatives are widely used in studies of purified membrane proteins but are difficult to solubilize in aqueous solution, even in the presence of detergent micelles. Other cholesterol derivatives do not form conventional micelles and lead to viscous solutions. To address these problems, a cholesterol-based detergent, CHOBIMALT, has been synthesized and characterized. At concentrations above 3?4 μM, CHOBIMALT forms micelles without the need for elevated temperatures or sonic disruption. Diffusion and fluorescence measurements indicated that CHOBIMALT micelles are large (210±30 kDa). The ability to solubilize a functional membrane protein was explored using a G-protein coupled receptor, the human kappa opioid receptor type 1 (hKOR1). While CHOBIMALT alone was not found to be effective as a surfactant for membrane extraction, when added to classical detergent micelles CHOBIMALT was observed to dramatically enhance the thermal stability of solubilized hKOR1. 相似文献
84.
Colin W. Hiebert Julian B. Thomas Brent D. McCallum D. Gavin Humphreys Ronald M. DePauw Matthew J. Hayden Rohit Mago Wendelin Schnippenkoetter Wolfgang Spielmeyer 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2010,121(6):1083-1091
Adult plant resistance (APR) to leaf rust and stripe rust derived from the wheat (Triticum aestivum L.) line PI250413 was previously identified in RL6077 (=Thatcher*6/PI250413). The leaf rust resistance gene in RL6077 is
phenotypically similar to Lr34 which is located on chromosome 7D. It was previously hypothesized that the gene in RL6077 could be Lr34 translocated to another chromosome. Hybrids between RL6077 and Thatcher and between RL6077 and 7DS and 7DL ditelocentric
stocks were examined for first meiotic metaphase pairing. RL6077 formed chain quadrivalents and trivalents relative to Thatcher
and Chinese Spring; however both 7D telocentrics paired only as heteromorphic bivalents and never with the multivalents. Thus,
chromosome 7D is not involved in any translocation carried by RL6077. A genome-wide scan of SSR markers detected an introgression
from chromosome 4D of PI250413 transferred to RL6077 through five cycles of backcrossing to Thatcher. Haplotype analysis of
lines from crosses of Thatcher × RL6077 and RL6058 (Thatcher*6/PI58548) × RL6077 showed highly significant associations between
introgressed markers (including SSR marker cfd71) and leaf rust resistance. In a separate RL6077-derived population, APR to stripe rust was also tightly linked with cfd71 on chromosome 4DL. An allele survey of linked SSR markers cfd71 and cfd23 on a set of 247 wheat lines from diverse origins indicated that these markers can be used to select for the donor segment
in most wheat backgrounds. Comparison of RL6077 with Thatcher in field trials showed no effect of the APR gene on important
agronomic or quality traits. Since no other known Lr genes exist on chromosome 4DL, the APR gene in RL6077 has been assigned
the name Lr67. 相似文献
85.
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87.
Christoph Kleinschnitz Henrike Grund Kirstin Wingler Melanie E. Armitage Emma Jones Manish Mittal David Barit Tobias Schwarz Christian Geis Peter Kraft Konstanze Barthel Michael K. Schuhmann Alexander M. Herrmann Sven G. Meuth Guido Stoll Sabine Meurer Anja Schrewe Lore Becker Valérie Gailus-Durner Helmut Fuchs Thomas Klopstock Martin Hrabé de Angelis Karin Jandeleit-Dahm Ajay M. Shah Norbert Weissmann Harald H. H. W. Schmidt 《PLoS biology》2010,8(9)
Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4
−/−) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4
−/− mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. 相似文献
88.
Functional specificity of a Hox protein mediated by the recognition of minor groove structure 总被引:2,自引:0,他引:2
Joshi R Passner JM Rohs R Jain R Sosinsky A Crickmore MA Jacob V Aggarwal AK Honig B Mann RS 《Cell》2007,131(3):530-543
89.
Padda BS Jung SA Pretorius D Nager CW Den-Boer D Mittal RK 《American journal of physiology. Gastrointestinal and liver physiology》2007,292(2):G565-G571
The role of pelvic floor muscle contraction in the genesis of anal canal pressure is not clear. Recent studies have suggested that vaginal distension increases pelvic floor muscle contraction. We studied the effects of vaginal distension on anal canal pressure in 15 nullipara asymptomatic women. Anal pressure, rest, and squeeze were measured using station pull-through manometry techniques with no vaginal probe, a 10-mm vaginal probe, and a 25-mm vaginal probe in place. Rest and squeeze vaginal pressures were significantly higher when measured with the 25-mm probe compared with the 10-mm probe, suggesting that vaginal distension enhances pelvic floor contraction. In the presence of the 25-mm vaginal probe, rest and squeeze anal pressures in the proximal part of the anal canal were significantly higher compared with no vaginal probe or the 10-mm vaginal probe. On the other hand, distal anal pressures were not affected by any of the vaginal probes. Ultrasound imaging of the pelvic floor revealed that vaginal distension increased the anterior-posterior length of the puborectalis muscle. Atropine at 15 micro g/kg had no influence on the rest and squeeze anal pressures with or without vaginal distension. Our data suggest that pelvic floor contractions increase pressures in the proximal part of the anal canal, which is anatomically surrounded by the puborectalis muscle. We propose that pelvic floor contraction plays an important role in the fecal continence mechanism by increasing anal canal pressure. 相似文献
90.
Mitochondrial reactive oxygen species signal hepatocyte steatosis by regulating the phosphatidylinositol 3-kinase cell survival pathway 总被引:2,自引:0,他引:2
Kohli R Pan X Malladi P Wainwright MS Whitington PF 《The Journal of biological chemistry》2007,282(29):21327-21336
Abnormal dietary intake of macronutrients is implicated in the development of obesity and fatty liver disease. Steatosis develops in cultured hepatocytes exposed to medium containing either a high concentration of long chain free fatty acids (HFFA) or medium deficient in methionine and choline (MCD). This study examined the mitochondrial reactive oxygen species (ROS)-dependent regulation of the phosphoinositol (PI) 3-kinase pathway in steatosis induced by exposure of AML-12 mouse hepatocytes to MCD or HFFA medium. Exposure to either MCD or HFFA medium resulted in increased production of superoxide anions and H(2)O(2), transduction of the PI 3-kinase pathway and steatosis. Inhibition of PI 3-kinase with LY294002 prevented steatosis. Pharmacologically inhibiting electron transport chain complex III production of ROS prevented activation of PI 3-kinase during macronutrient perturbation, whereas pharmacologically promoting electron transport chain complex III ROS production activated PI 3-kinase independent of nutrient input. The data suggest that H(2)O(2) is the ROS species involved in signal transduction; promoting the rapid conversion of superoxide to H(2)O(2) does not inhibit PI 3-kinase pathway activation during nutrient perturbation, and exogenous H(2)O(2) activates it independent of nutrient input. In addition to transducing PI 3-kinase, the ROS-dependent signal cascade amplifies the PI 3-kinase signal by maintaining phosphatase and tensin homolog in its inactive phosphorylated state. Knockdown of phosphatase and tensin homolog by small interfering RNA independently activated the PI 3-kinase pathway. Our findings suggest a common path for response to altered nutrition involving mitochondrial ROS-dependent PI 3-kinase pathway regulation, leading to steatosis. 相似文献