Exploring structural complexity in the discovery and self-assembly of a family of nanoscale chalcoxides from {Se8Mo36} to {Se26Mo68}

Herein, we show the controlled generation of multi-component libraries based on the [MoV2S2O2]2+/MoVIO42−/SeIVO32−/C4O42− system leading to the formation of a whole new family of nanosized molecular chalcoxides, {Se8Mo36} 1, {Se8Mo40} 2, {Se8Mo56} 3, {Se20Mo56} 4 and {Se26Mo68} 5, of the general formula {(MoV2O2S2)a(OH)b(SeIVO3)c(C4O4)d(MoVI2O7)e}n−, where a, b, c, d, e, n = [16, 20, 8, 6, 2, 20] for 1, [18, 24, 8, 6, 2, 20] for 2, [24, 32, 8, 8, 4, 24] for 3, [28, 32, 20, 8, 0, 32] for 4 and [34, 36, 26, 8, 0, 36] for 5. The coordination modulation effect offered by the SeIVO32− and the C4O42− anions lead to the generation of new building blocks, [(MoV2O2S2)3(OH)6(C4O4) (MoVI2O7)]4−, and the discovery of a new family of clusters of increasing nuclearity and complexity

The Influence of Tone Inventory on ERP without Focal Attention: A Cross-Language Study

This study investigates the effect of tone inventories on brain activities underlying pitch without focal attention. We find that the electrophysiological responses to across-category stimuli are larger than those to within-category stimuli when the pitch contours are superimposed on nonspeech stimuli; however, there is no electrophysiological response difference associated with category status in speech stimuli. Moreover, this category effect in nonspeech stimuli is stronger for Cantonese speakers. Results of previous and present studies lead us to conclude that brain activities to the same native lexical tone contrasts are modulated by speakers’ language experiences not only in active phonological processing but also in automatic feature detection without focal attention. In contrast to the condition with focal attention, where phonological processing is stronger for speech stimuli, the feature detection (pitch contours in this study) without focal attention as shaped by language background is superior in relatively regular stimuli, that is, the nonspeech stimuli. The results suggest that Cantonese listeners outperform Mandarin listeners in automatic detection of pitch features because of the denser Cantonese tone system

Photoproduction of nitric oxide in seawater

Nitric oxide (NO) is a short-lived intermediate of the oceanic nitrogen cycle. However, our knowledge about its production and consumption pathways in oceanic environments is rudimentary. In order to decipher the major factors affecting NO photochemical production, we irradiated several artificial seawater samples as well as 31 natural surface seawater samples in laboratory experiments. The seawater samples were collected during a cruise to the western tropical North Pacific Ocean (WTNP, a N-S section from 36 to 2 degrees N along 146 to 143 degrees E with 6 and 12 stations, respectively, and a W-E section from 137 to 161 degrees E along the Equator with 13 stations) from November 2015 to January 2016. NO photoproduction rates from dissolved nitrite in artificial seawater showed increasing trends with decreasing pH, increasing temperature, and increasing salinity. In contrast, NO photoproduction rates (average: 0.5 +/- 0.2 x 10(-12) mol L-1 s(-1)) in the natural seawater samples from the WTNP did not show any correlations with pH, water temperature, salinity, or dissolved inorganic nitrite concentrations. The flux induced by NO photoproduction in the WTNP (average: 13 x 10(-12) mol M-2 S-1) was significantly larger than the NO air-sea flux density (average: 1.8 x 10(-12) Mol M-2 S-1), indicating a further NO loss process in the surface layer

The effects of low frequency electrical stimulation on satellite cell activity in rat skeletal muscle during hindlimb suspension

<p>Abstract</p> <p>Background</p> <p>The ability of skeletal muscle to grow and regenerate is dependent on resident stem cells called satellite cells. It has been shown that chronic hindlimb unloading downregulates the satellite cell activity. This study investigated the role of low-frequency electrical stimulation on satellite cell activity during a 28 d hindlimb suspension in rats.</p> <p>Results</p> <p>Mechanical unloading resulted in a 44% reduction in the myofiber cross-sectional area as well as a 29% and 34% reduction in the number of myonuclei and myonuclear domains, respectively, in the soleus muscles (<it>P </it>< 0.001 <it>vs </it>the weight-bearing control). The number of quiescent (M-cadherin⁺), proliferating (BrdU⁺and myoD⁺), and differentiated (myogenin⁺) satellite cells was also reduced by 48-57% compared to the weight-bearing animals (<it>P </it>< 0.01 for all). Daily application of electrical stimulation (2 × 3 h at a 20 Hz frequency) partially attenuated the reduction of the fiber cross-sectional area, satellite cell activity, and myonuclear domain (<it>P </it>< 0.05 for all). Extensor digitorum longus muscles were not significantly altered by hindlimb unloading.</p> <p>Conclusion</p> <p>This study shows that electrical stimulation partially attenuated the decrease in muscle size and satellite cells during hindlimb unloading. The causal relationship between satellite cell activation and electrical stimulation remain to be established.</p

Spectra of Free Diquark in the Bethe-Salpeter Approach

In this work, we employ the Bethe-Salpeter (B-S) equation to investigate the spectra of free diquarks and their B-S wave functions. We find that the B-S approach can be consistently applied to study the diqaurks with two heavy quarks or one heavy and one light quarks, but for two light-quark systems, the results are not reliable. There are a few free parameters in the whole scenario which can only be fixed phenomenologically. Thus, to determine them, one has to study baryons which are composed of quarks and diquarks.Comment: 16 pages, no figure

XRCC1 and base excision repair balance in response to nitric oxide

Inflammation associated reactive oxygen and nitrogen species (RONs), including peroxynitrite (ONOO−) and nitric oxide (NOradical dot), create base lesions that potentially play a role in the toxicity and large genomic rearrangements associated with many malignancies. Little is known about the role of base excision repair (BER) in removing these endogenous DNA lesions. Here, we explore the role of X-ray repair cross-complementing group 1 (XRCC1) in attenuating RONs-induced genotoxicity. XRCC1 is a scaffold protein critical for BER for which polymorphisms modulate the risk of cancer. We exploited CHO and human glioblastoma cell lines engineered to express varied levels of BER proteins to study XRCC1. Cytotoxicity and the levels of DNA repair intermediates (single-strand breaks; SSB) were evaluated following exposure of the cells to the ONOO− donor, SIN-1, and to gaseous NOradical dot. XRCC1 null cells were slightly more sensitive to SIN-1 than wild-type cells. We used small-scale bioreactors to expose cells to NOradical dot and found that XRCC1-deficient CHO cells were not sensitive. However, using a molecular beacon assay to test lesion removal in vitro, we found that XRCC1 facilitates AAG-initiated excision of two key NOradical dot-induced DNA lesions: 1,N[superscript 6]-ethenoadenine and hypoxanthine. Furthermore, overexpression of AAG rendered XRCC1-deficient cells sensitive to NOradical dot-induced DNA damage. These results show that AAG is a key glycosylase for BER of NOradical dot-induced DNA damage and that XRCC1's role in modulating sensitivity to RONs is dependent upon the cellular level of AAG. This demonstrates the importance of considering the expression of other components of the BER pathway when evaluating the impact of XRCC1 polymorphisms on cancer risk.Massachusetts Institute of Technology. Center for Environmental Health Sciences (NIEHS P30-ES002109)National Institutes of Health (U.S.) (NIH grant P01-CA026731)National Institutes of Health (U.S.) (NIH grant 2-R01-CA079827-05A1)National Institutes of Health (U.S.) (NIH Grant U01-ES016045)National Institutes of Health (U.S.) (NIH Grant GM087798)National Institutes of Health (U.S.) (NIH Grant CA148629)National Institutes of Health (U.S.) (NIH Grant ES019498)National Institutes of Health (U.S.) (Cancer Center Support Grant P30 CA047904