1,658 research outputs found
Distribution of partial credit given to different authors for an imaginary publication with 1–10 authors with one first author and one corresponding author<sup>#</sup>.
No full text<p>: The first and corresponding author is the same.</p><p>#: The last author has been assumed to be the corresponding author.</p
O−H···O versus O−H···S Hydrogen Bonding. 3. IR−UV Double Resonance Study of Hydrogen Bonded Complexes of <i>p</i>-Cresol with Diethyl Ether and Its Sulfur Analog
No full textIn this work the hydrogen bonded complexes of diethyl ether (DEE) and diethyl sulfide (DES) with p-cresol (p-CR) were investigated. Only one conformer of the p-CR·DEE complex and three conformers of the p-CR·DES complex were found to be present under the supersonic jet expansion conditions. The conformational assignments were done with the help of IR−UV double resonance studies and ab initio calculations. The red shifts in the OH stretching frequency for the O−H···O and O−H···S hydrogen bonded complexes were quite close to each other. In fact, one of the p-CR·DES conformers showed a slightly larger red shift in the OH stretch than that in the p-CR·DEE conformer, which suggests that in this case sulfur is not a weak hydrogen bond acceptor as noted previously in case of the p-CR·H2O and p-CR·H2S complexes (Biswal et al. J. Phys. Chem. A 2009, 113, 5633). The natural bond orbital analysis also shows that the extent of overlap between sulfur lone pair orbitals (LP) and OH antibonding orbital (σ*OH) was comparable to the oxygen (LP) and σ*OH overlap, consistent with the similar magnitudes of the red shifts of OH stretch in the DES and DEE complexes. The computed binding energy of the p-CR·DES complex, however, was about 80% of the p-CR·DEE complex. The electron densities at the bond critical points indicated that the O−H···S interaction was weaker than the O−H···O interaction in this particular system also. The important finding of this study was that the IR red shifts in the H-bond donor X−H stretching frequency were not quite consistent with the computed binding energies and the atoms-in-molecules analysis contrary to the general understanding. Energy decomposition analysis suggests that O−H···S hydrogen bonding interaction is dispersive in nature and the dispersion contribution decreases with the increase in the length of the alkyl chain of the “S” hydrogen bond acceptor
The partial credit (a<sub>0</sub>) given to the primary author for articles with 1–100 imaginary authors.
No full text<p>The partial credit (a<sub>0</sub>) given to the primary author for articles with 1–100 imaginary authors.</p
Correlation of <i>Ab-</i>, h- and w-indices with the percentage of credit earned as primary author.
No full text<p>The correlation of <i>Ab-</i>, h- and w-indices to the percentage of credit earned as the primary author of ten individuals randomly chosen from top-20 highly cited authors in the field of Molecular Biology & Genetics of the year 2010 (data source: Thomson Reuters Essential Science IndicatorsSM).</p
Nrf2 deficiency influences susceptibility to steroid resistance via HDAC2 reduction
No full textAbnormal lung inflammation and oxidant burden are associated with a significant reduction in histone deacetylase 2 (HDAC2) abundance and steroid resistance. We hypothesized that Nrf2 regulates steroid sensitivity via HDAC2 in response to inflammation in mouse lung. Furthermore, HDAC2 deficiency leads to steroid resistance in attenuating lung inflammatory response, which may be due to oxidant/antioxidant imbalance. Loss of antioxidant transcription factor Nrf2 resulted in decreased HDAC2 level in lung, and increased inflammatory lung response which was not reversed by steroid. Thus, steroid resistance or inability of steroids to control lung inflammatory response is dependent on Nrf2-HDAC2 axis. These findings have implications in steroid resistance, particularly during the conditions of oxidative stress when the lungs are more susceptible to inflammatory response, which is seen in patients with chronic obstructive pulmonary disease, asthma, rheumatoid arthritis, and inflammatory bowel disease
Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease
No full textChronic obstructive pulmonary disease (COPD) is a global health problem. The current therapies for COPD are poorly effective and the mainstays of pharmacotherapy are bronchodilators. A better understanding of the pathobiology of COPD is critical for the development of novel therapies. In the present review, we have discussed the roles of oxidative/aldehyde stress, inflammation/immunity, and chromatin remodeling in the pathogenesis of COPD. An imbalance of oxidants/antioxidants caused by cigarette smoke and other pollutants/biomass fuels plays an important role in the pathogenesis of COPD by regulating redox-sensitive transcription factors (e.g., NF-κB), autophagy and unfolded protein response leading to chronic lung inflammatory response. Cigarette smoke also activates canonical/alternative NF-κB pathways and their upstream kinases leading to sustained inflammatory response in lungs. Recently, epigenetic regulation has been shown to be critical for the development of COPD because the expression/activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in airways of COPD patients. Hence, the significant advances made in understanding the pathophysiology of COPD as described herein will identify novel therapeutic targets for intervention in COPD
Study of Bc+→J/ψDs+ and Bc+→J/ψDs∗+ decays in pp collisions at √s = 13 TeV with the ATLAS detector
No full textA study of Bc+→J/ψDs+ and Bc+→J/ψDs∗+ decays using 139 fb−1 of integrated luminosity collected with the ATLAS detector from s = 13 TeV pp collisions at the LHC is presented. The ratios of the branching fractions of the two decays to the branching fraction of the Bc+→ J/ψπ+ decay are measured: B(Bc+→J/ψDs+)/B(Bc+→J/ψπ+) = 2.76 ± 0.47 and B(Bc+→J/ψDs∗+)/B(Bc+→J/ψπ+) = 5.33 ± 0.96. The ratio of the branching fractions of the two decays is found to be B(Bc+→J/ψDs∗+)/B(Bc+→J/ψDs∗+) = 1.93 ± 0.26. For the Bc+→J/ψDs∗+ decay, the transverse polarization fraction, Γ±±/Γ, is measured to be 0.70 ± 0.11. The reported uncertainties include both the statistical and systematic components added in quadrature. The precision of the measurements exceeds that in all previous studies of these decays. These results supersede those obtained in the earlier ATLAS study of the same decays with s = 7 and 8 TeV pp collision data. A comparison with available theoretical predictions for the measured quantities is presented. [Figure not available: see fulltext.]
Environmental toxicity, redox signaling and lung inflammation:the role of glutathione
No full textGlutathione (gamma-glutamyl-cysteinyl-glycine, GSH) is the most abundant intracellular antioxidant thiol and is central to redox defense during oxidative stress. GSH metabolism is tightly regulated and has been implicated in redox signaling and also in protection against environmental oxidant-mediated injury. Changes in the ratio of the reduced and disulfide form (GSH/GSSG) can affect signaling pathways that participate in a broad array of physiological responses from cell proliferation, autophagy and apoptosis to gene expression that involve H(2)O(2) as a second messenger. Oxidative stress due to oxidant/antioxidant imbalance and also due to environmental oxidants is an important component during inflammation and respiratory diseases such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, acute respiratory distress syndrome, and asthma. It is known to activate multiple stress kinase pathways and redox-sensitive transcription factors such as Nrf2, NF-kappaB and AP-1, which differentially regulate the genes for pro-inflammatory cytokines as well as the protective antioxidant genes. Understanding the regulatory mechanisms for the induction of antioxidants, such as GSH, versus pro-inflammatory mediators at sites of oxidant-directed injuries may allow for the development of novel therapies which will allow pharmacological manipulation of GSH synthesis during inflammation and oxidative injury. This article features the current knowledge about the role of GSH in redox signaling, GSH biosynthesis and particularly the regulation of transcription factor Nrf2 by GSH and downstream signaling during oxidative stress and inflammation in various pulmonary diseases. We also discussed the current therapeutic clinical trials using GSH and other thiol compounds, such as N-acetyl-l-cysteine, fudosteine, carbocysteine, erdosteine in environment-induced airways disease
Task modulated brain connectivity of the amygdala: a meta-analysis of psychophysiological interactions
No full text
Understanding functional connectivity of the amygdala with other brain regions, especially task modulated connectivity, is a critical step toward understanding the role of the amygdala in emotional processes and the interactions between emotion and cognition. The present study performed coordinate-based meta-analysis on studies of task modulated connectivity of the amygdala which used psychophysiological interaction (PPI) analysis. We first analyzed 49 PPI studies on different types of tasks using activation likelihood estimation (ALE) meta-analysis. Widespread cortical and subcortical regions showed consistent task modulated connectivity with the amygdala, including the medial frontal cortex, bilateral insula, anterior cingulate, fusiform gyrus, parahippocampal gyrus, thalamus, and basal ganglia. These regions were in general overlapped with those showed coactivations with the amygdala, suggesting that these regions and amygdala are not only activated together, but also show different levels of interactions during tasks. Further analyses with subsets of PPI studies revealed task specific functional connectivities with the amygdala that were modulated by fear processing, face processing, and emotion regulation. These results suggest a dynamic modulation of connectivity upon task demands, and provide new insights on the functions of the amygdala in different affective and cognitive processes. The meta-analytic approach on PPI studies may offer a framework toward systematical examinations of task modulated connectivity.</p
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