Analysis of corrections to the eikonal approximation

Various corrections to the eikonal approximations are studied for two- and three-body nuclear collisions with the goal to extend the range of validity of this approximation to beam energies of 10 MeV/nucleon. Wallace's correction does not improve much the elastic-scattering cross sections obtained at the usual eikonal approximation. On the contrary, a semiclassical approximation that substitutes the impact parameter by a complex distance of closest approach computed with the projectile-target optical potential efficiently corrects the eikonal approximation. This opens the possibility to analyze data measured down to 10 MeV/nucleon within eikonal-like reaction models.Comment: 10 pages, 8 figure

Image1_Development and validation of a nomogram for predicting cardiovascular mortality risk for diffuse large B-cell lymphoma in children, adolescents, and adults.tif

ObjectiveThis study aimed to construct and validate a nomogram for predicting cardiovascular mortality (CVM) for child, adolescent, and adult patients with diffuse large B-cell lymphoma (DLBCL).Materials and methodsPatients with only one primary tumor of DLBCL first diagnosed between 2000 and 2019 in the SEER database were extracted. We used the cumulative incidence function (CIF) to evaluate the cumulative rate of CVM. The outcome of interest was CVM, which was analyzed using a competing risk model, accounting for death due to other causes. The total database was randomly divided into a training cohort and an internal validation cohort at a ratio of 7:3. Adjustments were for demographics, tumor characteristics, and treatment modalities. Nomograms were constructed according to these risk factors to predict CVM risk at 5, 10, and 15 years. Validation included receiver operating characteristic (ROC) curves, time-dependent ROC, C-index, calibration curves, and decision curve analysis.ResultsOne hundred four thousand six hundred six patients following initial diagnosis of DLBCL were included (58.3% male, median age 64 years, range 0–80, White 83.98%). Among them, 5.02% died of CVM, with a median follow-up time of 61 (31–98) months. Nomograms based on the seven risk factors (age at diagnosis, gender, race, tumor grade, Ann Arbor stage, radiation, chemotherapy) with hazard ratios ranging from 0.19–1.17 showed excellent discrimination, and calibration plots demonstrated satisfactory prediction. The 5-, 10-, and 15-year AUC and C-index of CVM in the training set were 0.716 (0.714–0.718), 0.713 (0.711–0.715), 0.706 (0.704–0.708), 0.731, 0.727, and 0.719; the corresponding figures for the validation set were 0.705 (0.688–0.722), 0.704 (0.689–0.718), 0.707 (0.693–0.722), 0.698, 0.698, and 0.699. Decision curve analysis revealed a clinically beneficial net benefit.ConclusionsWe first built the nomogram model for DLBCL patients with satisfactory prediction and excellent discrimination, which might play an essential role in helping physicians enact better treatment strategies at the time of initial diagnosis.</p

Transcriptional expression of cardiac development-related transcription factors in cardiac progenitor cells after lentivirus transfeciton with Islet-1 RNAi.

<p>Quantitative RT-PCR analysis showed the mRNA level for Islet-1 was dramatically reduced in cardiac progenitor cells when transfected with Islet-1 RNA interference vector to inhibit Islet-1 (A). The mRNA levels for Mef2c and Tbx5 were significantly reduced in the cells when Islet-1 expression was inhibited with RNAi as compared with the controls. There was no significant difference in GATA4 mRNA level in the cells with Islet-1 knockdown with RNAi (B). *<i>p</i> < 0.05, n=3-5. </p

Acetylation level of histone H3 in cardiac progenitor cells after inhibiting Islet-1 expression.

<p>Western blotting analysis showed that detectable level of histone H3 acetylation was present in cardiac progenitor cells, and was not significantly changed when Islet-1 expression was inhibited (A, <i>p</i>>0.05, n=3). However, the DNA quantity of Mef2c in the promoter region immunoprecipitated with acH3 antibody was significantly decreased in the cells transfected with Islet-1 RNAi as compared with the controls, while no difference was observed in the DNA quantity of GATA4 and Tbx5 in the cells (B). *<i>p</i><0.05, n=3. </p

Expression of Islet-1 protein in mouse embryonic and neonatal hearts.

<p>A representative Western blotting showed that Islet-1 was dynamically expressed in the embryonic hearts. The expression of Islet-1 in mouse embryonic hearts was significantly higher on E14.5 than that on E11.5, E17.5, and neonatal mice. * <i>p</i> < 0.05 (n=3).</p

Interaction of p300 with the promoter regions of Mef2c, GATA4 and Tbx5 in cardiac progenitor cells.

<p>The DNA quantity of Mef2c in the promoter regions immunoprecipitated using p300 antibody was significantly decreased in the cells transfected with Islet-1 RNAi as compared with the controls. However, no difference in the DNA quantity of GATA4 and Tbx5 was observed in the cells with or without transfection with Islet-1 RNAi. * <i>p</i> < 0.05, n=3.</p

Association of Two Variants in <i>SMAD7</i> with the Risk of Congenital Heart Disease in the Han Chinese Population

<div><p>SMAD7 is a general antagonist of TGF-β signaling and has been found to be involved in cardiogenesis in mouse models, but its role in human congenital heart disease (CHD) has yet to be investigated. To examine if <i>SMAD7</i> is associated with CHD, we conducted a case-control study in the Han Chinese population. Exon1 and exon4 of <i>SMAD7</i>, which encode the functional MH1 and MH2 domains, were directly sequenced in 1,201 sporadic CHD patients and 1,116 control individuals. A total of 18 sequence variations were identified. Two common variants rs3809922 and rs3809923 are located at exon4 of SMAD7, and were found in strong linkage disequilibrium with each other (<i>r</i>² = 0.93). We analyzed the association of these two loci with CHD in 3 independent subgroup case-control studies, and found that in some subgroups, rs3809922 and rs3809923 were significantly associated with CHD through genetic model analysis. In the combined data set, TT genotype in rs3809922 significantly increased the risk of CHD compared with CC and CT, while GG genotype in rs3809923 significantly increased the risk of CHD compared with CC and CG, particularly in the recessive model. In addition, haplotype analyses showed that haplotype TG significantly increased the risk of CHD (<i>P</i> = 6.9×10⁻⁶); this finding supports the results from the analyses based on single locus. According to data from the 1000 Genomes Project, the frequencies of the two risk alleles varied greatly between populations worldwide, which indicate the identified associations might have a population difference. To our knowledge, this is the first report that genetic variants in <i>SMAD7</i> influence susceptibility to CHD risk.</p></div

<i>SMAD7</i> sequence variants identified in CHD and control subjects.

a<p>These columns indicate the number of heterozygotes. Where there are two numbers, the first represents the number of heterozygotes, and the second represents the number of homozygotes.</p>b<p>Common variations with minor allele frequencies (MAF) ≥10%; others variations are rare mutations with MAF <1%.</p

A region that was in extremely strong LD with rs3809922 and rs3809923.

<p>Each box represents the LD relationship between two SNPs. The strength of the LD was shown in increasing of red for higher LOD score which indicated higher LD. The white line on the top represents the relative physical position of the SNPs on the chromosome. The value in each box was the |D'| (×100) between each pair of SNPs, another statistics to measure LD.</p

Association of rs3809922 and rs3809923 variants with septation defects.

<p>All the P-values were calculated based on the χ² test unless otherwise indicated.</p>#<p>, degrees of freedom  = 2;</p>*<p>, P-value was calculated based on the Cochran–Armitage test.</p