Time-dependent energetic proton acceleration and scaling laws in ultra-intense laser pulses interactions with thin foils

A two-phase model, where the plasma expansion is an isothermal one when laser irradiates and a following adiabatic one after laser ends, has been proposed to predict the maximum energy of the proton beams induced in the ultra-intense laser-foil interactions. The hot-electron recirculation in the ultra-intense laser-solid interactions has been accounted in and described by the time-dependent hot-electron density continuously in this model. The dilution effect of electron density as electrons recirculate and spread laterally has been considered. With our model, the scaling laws of maximum ion energy have been achieved and the dependence of the scaling coefficients on laser intensity, pulse duration and target thickness have been obtained. Some interesting results have been predicted: the adiabatic expansion is an important process of the ion acceleration and cannot be neglected; the whole acceleration time is about 10-20 times of laser pulse duration; the larger the laser intensity, the more sensitive the maximum ion energy to the change of focus radius, and so on.Comment: 15 pages, 4 figures, submitted to PR

Genomic insights and prognostic significance of novel biomarkers in pancreatic ductal adenocarcinoma: A comprehensive analysis

Pancreatic ductal adenocarcinoma (PDAC) is a highly prevalent digestive system malignancy, with a significant impact on public health, especially in the elderly population. The advent of the Human Genome Project has opened new avenues for precision medicine, allowing researchers to explore genetic markers and molecular targets for cancer diagnosis and treatment. Despite significant advances in genomic research, early diagnosis of pancreatic cancer remains elusive due to the lack of highly sensitive and specific markers. Therefore, there is a need for in-depth research to identify more precise and reliable diagnostic markers for pancreatic cancer. In this study, we utilized a combination of public databases from different sources to meticulously screen genes associated with prognosis in pancreatic cancer. We used gene differential analysis, univariate cox regression analysis, least absolute selection and shrinkage operator (LASSO) regression, and multivariate cox regression analysis to identify genes associated with prognosis. Subsequently, we constructed a scoring system, validated its validity using survival analysis and ROC analysis, and further confirmed its reliability by nomogram and decision curve analysis (DCA). We evaluated the diagnostic value of this scoring system for pancreatic cancer prognosis and validated the function of the genes using single cell data analysis. Our analysis identifies six genes, including GABRA3, IL20RB, CDK1, GPR87, TTYH3, and KCNA2, that were strongly associated with PDAC prognosis. Clinical prognostic models based on these genes showed strong predictive power not only in the training set but also in external datasets. Functional enrichment analysis revealed significant differences between high- and low-risk groups mainly in immune-related functions. Additionally, we explored the potential of the risk score as a marker for immunotherapy response and identified key factors within the tumor microenvironment. The single-cell RNA sequencing analysis further enriched our understanding of cell clusters and six hub genes expressions. This comprehensive investigation provides valuable insights into pancreatic PDAC and its intricate immune landscape. The identified genes and their functional significance underscore the importance of continued research into improving diagnosis and treatment strategies for PDAC

MicroRNA-572 Improves Early Post-Operative Cognitive Dysfunction by Down-Regulating Neural Cell Adhesion Molecule 1

<div><p>Post-operative cognitive dysfunction (POCD) is a commonly-seen postoperative complication in elderly patients. However, the underlying mechanisms of POCD remain unclear. miRNAs, which are reported to be involved in the pathogenesis of the nervous system diseases, may also affect POCD. In this study, miRNA microarray technology was used to analyze the circulating miRNA expression profile of POCD patients. Among the altered miRNAs, miR-572 had the greatest decrease, which was also verified <i>in vivo</i> in rat POCD model. Further analysis found that miR-572 could regulate the expression of NCAM1 in the hippocampal neurons and interfering miR-572 expression could facilitate the restoration of cognitive function <i>in vivo.</i> Moreover, clinical correlation analysis found that the miR-572 expression was associated with the incidence of POCD. Collectively, miR-572 is involved in the development and restoration of POCD and it may serve as a biological marker for early diagnosis of POCD.</p></div

miR-572 expression in the peripheral blood of clinical patients.

<p>A. Real-time quantitative PCR detection of the miR-572 expression levels in the peripheral blood of POCD patients (n = 38) before surgery (Pre), 24 h after surgery (Pos-24h), and 7 days after surgery (Pos-7d). B. Real-time quantitative PCR detection of the miR-572 expression levels in the peripheral blood of non-POCD patients (n = 62) before surgery (Pre), 24 h after surgery (Pos-24h), and 7 days after surgery (Pos-7d). C. Real-time quantitative PCR detection of the miR-572 expression levels in the peripheral blood of POCD patients whose cognitive function was recovered 3 months after surgery (n = 29, Group1) and whose cognitive function was not recovered (n = 9, Group2) 24 h after surgery. D. Real-time quantitative PCR detection of the miR-572 expression levels in the peripheral blood of POCD patients whose cognitive function was recovered 3 months after surgery (n = 29, Group1) and whose cognitive function was not recovered (n = 9, Group2) 7 days after surgery.</p

Targeted regulation of the expression of NCAM by miR-572.

<p>A. Schematics of miR-572 binding to the 3'UTR region of the NCAM1 mRNA (wildtype and mutant) in the dual-luciferase experiment. B. The dual-luciferase assay showed that miR-572 significantly reduced the luciferase activity of plasmids containing the wildtype 3'UTR region of mouse NCAM1 mRNA. C. Overexpression of miR-572 in mouse HT22 cells could significantly reduce the NCAM1 expression at the mRNA and protein levels. D. Inhibition of miR-572 in mouse HT22 cells could significantly promote NCAM1 expression at the mRNA and protein levels. E. Immunohistochemical detection showed that after inhibiting miR-572 expression in the POCD rat brain, the NCAM1 expression was elevated. WT, wildtype; MUT, mutant; NC, negative control.</p

Primers Sequence.

<p>Primers Sequence.</p