Data for: Vocal Attractiveness and Naturally Pitch-Shifted Voices

Data from the study titled "Vocal attractiveness and voluntarily pitch-shifted voices"

Bank loan covenants, lending relationships and covenant violations

Using a large sample of U.S. corporate bank loans, we investigate the influence of lending relationships on loan covenants and covenant violations. Consistent with the information asymmetry argument, we find that lending relationships substitute for financial covenants in loan contracts. In addition, the effect of lending relationship intensity on the total number of financial covenants included in a loan package is U-shaped. It appears that lending relationship intensity acts as an indicator of covenant violations. Specifically, an increasing lending relationship intensity decreases the likelihood of covenant violations, but relationship borrowers who have access to the public debt market or are of a large size in their industry are subject to a high probability of covenant violations. Overall, relationship borrowers with different levels of relationship intensity and financing capacity are subject to a distinct probability of covenant violations

VIDEO ANALYSIS AND 3D DETECTION SIMULATION OF JUMP SHOT PRECISION FOR BASKETBALL PLAYERS

ABSTRACT With the rapid development and application of computer technology, the application of computer science knowledge in basketball is also more and more extensive. Based on genetic algorithm and the background subtraction method, video analysis and 3D detection simulation model of shot jump action precision were constructed in this study. According to the genetic algorithm search method, jump shot precision was analyzed, and the problems encountered in the actual shooting process of basketball players were studied and solved. The results show that this study is necessary and feasible.</div

Cdc42 deletion in HRasV12-driven tumors inhibits tumor growth.

<p>(<b>a</b>) HRasV12; Cdc42^f/f cells were transduced with retroviral ER-Cre and selected with puromycin. Antibiotic resistant cells were pooled and treated in culture with 4-OH Tamoxifen (4-OHT) or vehicle. Recombination at the <i>cdc42</i> locus was determined by PCR. (<b>b</b>) Cell lysates were isolated from cells cultured in the presence and absence of 4-OHT. Western blotting was performed to determine Cdc42 protein levels following Tamoxifen-induced recombination. (<b>c</b>) HRasV12; ER-Cre; Cdc42^f/f and HRasV12; Cdc42^f/f cells were injected into the flanks of immunocompromised nude mice. Five days post-injection, palpable tumors had formed and mice were administered 100 µl of 10 mg/ml 4-OHT in sunflower seed oil or vehicle control once a day, five days a week for 3 weeks. Tumor volume was monitored by caliper measurements. n = 8. (<b>d</b>) At 25 days post-injection, mice were sacrificed and tumors excised and weighed. A representative image of 4 HRasV12; ER-Cre; Cdc42f/f tumors treated with either tamoxifen or vehicle control is shown. (<b>e</b>) Genotyping was performed on DNA isolated from HRasV12; ER-Cre; Cdc42^f/f tumors treated with either vehicle or 4-OHT to determine the status of the <i>cdc42</i> locus. A representative image of genotyping results from two mice per condition (two tumors per mouse) is shown. Densitometry was performed using imageJ software and the intensity of the recombined <i>cdc42</i> allele relative to the non-recombined <i>cdc42</i> allele is plotted.</p

Cdc42 loss does not impair transformation by the oncoprotein, c-Myc.

<p>(<b>a</b>) p53-immortalized cells were infected with a retrovirus expressing the oncoprotein, c-Myc. c-Myc overexpression was verified by western blot analysis. (<b>b</b>) Pull-down assays were performed with GST-PAK1 to determine the relative abundance of activated Cdc42 in HRasV12 vs. c-Myc transformed cells. (<b>c</b>) Lysates from c-Myc transformed cells infected with Ad-GFP or Ad-GFP-Cre were immunoblotted for Cdc42. (<b>d</b>) Cultured c-Myc transformed cells were visualized 4 days following <i>cdc42</i> deletion by bright field microscopy (upper 2 panels). Cells were fixed and stained with rhodamine-phalloidin and DAPI to visualize actin structures (lower 2 panels). (<b>e</b>) An equal number of c-Myc transformed Cdc42 proficient and deficient cells were seeded. Cells were counted every three days by trypan blue exclusion. Curves represent at least two independent experiments performed in triplicate. (<b>f</b>) Cdc42-proficient and –deficient c-Myc cells were grown in a 0.3% agarose solution. Experiments were performed in triplicate and 9 independent fields were counted for colonies. ns = not significant.</p

Tuning the Catalytic Activity of Synthetic Enzyme KE15 with DNA

Efficiency improvement of synthetic enzymes through scaffold modifications suffers from limitations in terms of effectiveness, cost, and potential devastating consequences for protein structural stability. Here, we propose an alternative to scaffold modification, within electrostatic preorganization theory, where the enzyme’s greater environment is designed to support the evolution of the reaction in the active site. We demonstrate the feasibility of such an approach by placing a (polar) DNA fragment in the surroundings of the Kemp eliminase enzyme KE15 (structure from Houk’s group) and computing the resulting change in catalytic activity. We find that the introduction of a DNA fragment magnifies the contribution of protein residues to the stabilization of the transition state, estimated from electric field calculations with polarizable molecular dynamics. Our randomly generated test systems reveal a 2.0 kcal/mol reduction in activation energy, suggesting that even more significant catalytic improvements could be made by optimizing DNA size, sequence, and orientation with respect to the enzyme, validating our approach

Impact of Finer Grid Resolution on the Spatial Distribution of Vehicle Emissions Inventories

The ability to model air quality dispersion at increasingly smaller resolutions requires a concomitant improvement in the resolution of the gridded mobile source emissions used as input to these models. Two methods are currently used to allocate mobile emissions to grids; because of the limitations associated with these methods, their application is usually restricted to coarser grid resolutions. This paper uses a new mobile emissions inventory model (UCDrive) to explore the spatial distribution of mobile source emissions using finer grid cell resolutions. Our results indicate that the new model improves the precision of the spatial allocation of mobile source emissions, which in turn improves our ability to identify and implement pollutant control strategies

Cdc42 deletion in HRasV12 transformed cells results in dramatic morphological changes and deregulation of Cdc42 effector pathways.

<p>(<b>a</b>) Recombination of the cdc42 locus following addition of Cre recombinase was monitored by genomic PCR detecting the loxp allele. (<b>b</b>) Recombination of the cdc42 locus correlates with loss of Cdc42 protein expression as determined by western blot analysis. (<b>c</b>) Cultured HRasV12 cells and non-transformed cells were visualized 4 days following cdc42 deletion by bright field microscopy (upper 4 panels). Cells were fixed and stained with rhodamine-phalloidin and 4,6-diamidino-2-phenylindole (DAPI) to visualize actin structures. (<b>d</b>) Cell lysates from Ad-GFP-Cre and control infected cells were immunoblotted for proteins involved in effector signaling downstream of activated Cdc42.</p

Cdc42 activity is increased upon Ras-mediated transformation.

<p>(<b>a</b>) Cell immortalization was achieved following retroviral transduction of cdc42^f/f cells with a dominant-negative p53 (p53dd). Dominant-negative expression was determined by western blot for p53. (<b>b</b>) Immortalized, cdc42^f/f cells were transformed through retroviral transduction with HRasV12. Transformed cells exhibit HRas overexpression and increased active, GTP-bound HRas as determined by pull-down with the ras binding domain (RBD) of Raf1 fused to GST. (<b>c</b>) HRasV12 transformed cells exhibit a significant increase in Cdc42 activity compared to non-transformed control cells. Pull-down assays were performed with GST-PAK1. The graphed data represents densitometry quantification from three independent experiments.</p

Cdc42-deficiency impairs HRasV12-driven tumorigenesis.

<p>(<b>a</b>) Cdc42 proficient and deficient cells in a 1∶1 PBS:matrigel mixture were subcutaneously injected into the flanks of immunocompromised nude mice. Developing tumors were measured at indicated time points with calipers to determine tumor volume. n = 6. (<b>b</b>) 16 days post-injection mice were sacrificed and tumors excised and weighed (upper panel). A representative image of tumors from three mice are shown (lower panel). (<b>c</b>) Tumors were fixed, sectioned and stained with hematoxylin and eosin. (<b>d</b>) Left panel - The recombination status of the <i>cdc42</i> locus was determined for cells prior to injection into nude mice by genomic PCR. Right panel - DNA was isolated from resulting subcutaneous tumors and the recombination status of <i>cdc42</i> determined by PCR. Tumors from two representative mice were shown. The upper band corresponds to the non-recombined loxp/loxp allele from injected cells, the middle band corresponds to the wild-type <i>cdc42</i> allele derived from stromal cells derived from the recipient mouse, and the lower band corresponds to the recombined <i>cdc42</i> allele.</p