Self-compression of femtosecond laser pulses in ambient air

We demonstrate the self-compression of 98 fs near-infrared laser pulses down to 8.8 fs in ambient air, utilizing self-phase modulation in air and negative dispersion in the properties of a laser-induced plasma. The blue-shifted pulses achieve self-compression through conical radiation, eliminating the need for additional dispersion compensation. The results highlight a simple and compact approach to generate sub-10 fs laser pulses without additional measures for time-resolved applications in ultrafast diagnostics and spectroscopy

Study on the Deactivation of V₂O₅–WO₃/TiO₂ Selective Catalytic Reduction Catalysts through Transient Kinetics

The mechanism underlying the deactivation of a commercial V₂O₅–WO₃/TiO₂ catalyst for NH₃ selective catalytic reduction (SCR) of NO_<i>x</i> through exposure to the flue gas of a coal-fired power plant was investigated by a transient kinetic analysis that focused on the distinction between the deactivation behaviors of adsorption sites and redox sites. The results showed that alkali dopants preferentially poison the active sites associated with vanadium (V⁵⁺–OH and/or V⁵⁺O) rather than the sites associated with titania and tungsten. Obvious changes in the activation energies for NH₃ desorption, oxidation, and SCR surface reaction over the used catalyst were observed. Kinetic variations showed that three other factors that are involved in the elementary surface steps are responsible for the catalyst deactivation rather than simply the decline of the NH₃ adsorption capacity. Finally, the effects of these factors on the catalyst activity were analyzed at different temperatures

BikDDA eliminated TNBC cells more powerfully than BikDD.

<p>A. S124A and previous mutant sites T33D and S35D didn’t locate in the pro-apoptotic region of Bik. B. MDA-MB-231 cells were transfected for 28h with the same amount of pUK21, pUK21-BikDD or pUK21-BikDDA. Apoptotic cells were monitored by Annexin V/PI staining and flow-cytometry analysis. The right-lower or right upper quadrant of each plot showed early apoptotic or late apoptotic cells. C. Histogram directly showed the enhanced apoptosis-inducing activity of BikDDA. D. The cytotoxicity of BikDD and BikDDA were analyzed by Cell counting kit and MTT assay (setting at 100% in vector group). E. Western blotting was performed to confirm the prolonged half-life of BikDDA in 231 cells. F. MEK1/2 inhibitor UO126 and selective ERK1/2 inhibitor FR180204 increased the stability of BikDD in 231 cells.</p

Univariate and multivariate analysis for prognostic value of p-ERK1/2 expression in breast cancer patients.

<p>a: lymph node; b: negative; c: positive.</p

High levels of p-ERK1/2 correlated with loss of Bik and overexpression of Bcl-Xl and Mcl-1.

<p>High levels of p-ERK1/2 correlated with loss of Bik and overexpression of Bcl-Xl and Mcl-1.</p

BikDDA had a longer half-life than BikDD.

<p>A. 293 cells were transfected for 16h with same amount of pUK21- BikDD or pUK21-BikDDA and treated with protein biosynthesis inhibitor cycloheximide (CHX), proteasome inhibitor MG132 or Mek1/2 inhibitor UO126. B. Histogram and line charts showed the gray scale quantitative analysis for western blotting using Gel-pro software. The relative levels before CHX treatment were set as 100%. These results demonstrated that BikDDA degradation rate was lower than BikDD.</p

Higher p-ERK1/2 correlated with 5-FU resistance and BIKDDA could enhance the cytotoxicity of 5-FU.

<p>A. Kaplan-Meier curve of disease-free survival showed the decreased disease-free survival time of high p-ERK1/2 group who received adjuvant 5-FU based chemotherapy than the low. B and C. High levels of p-ERK1/2 correlated with 5-FU resistance (patients with metastasis and/or recurrence after adjuvant 5-FU based chemotherapy). After stratified by lymph node metastasis the correlation also exhibited statistics significance in metastasis positive cohort. D. 435 and 231 cells were transfected with vector control or BikDDA in combination with 25 ug/ml 5-FU or not, 24h later cell viability was analyzed by MTT assay (vector transfected only setting as 100%). These data showed BIKDDA can enhance the cytotoxicity of 5-FU.</p

BikDDA, a Mutant of Bik with Longer Half-Life Expression Protein, Can Be a Novel Therapeutic Gene for Triple-Negative Breast Cancer

<div><p>Our previous studies showed that BikDD, a constitutively active mutant form of Bik, exhibited powerful antitumor effects in preclinical pancreatic, lung and breast cancer models. Howerver, the antitumor activity of BikDD in triple-negative breast cancer (TNBC) is unknown. Here we show that aberrant expression of p-ERK1/2 was a meaningful molecular phenotype in TNBC patients, and can be an obstacle for treatment because of the converse correlation with Bik. A novel mutant, BikDDA, in which Ser¹²⁴ was changed to Alanine to block BikDD phosphorylation by p-ERK1/2 prevented subsequent ubiquitin-proteasome degradation. BikDDA showed a prolonged half-life and enhanced pro-apoptotic ability in TNBC cells compared with BikDD. Moreover, aberrant expression of p-ERK1/2 was associated with 5-fluorouracil resistance in breast cancer patients and BikDDA enhanced the therapeutic effects of 5-fluorouracil in vitro.</p></div

Generation of 210 GW few-cycle ultraviolet laser pulses

We demonstrate generation, spectral broadening, and post-compression of ultraviolet pulses using a thin BBO crystal on a fused silica substrate as the nonlinear interaction medium. By combining the second harmonic generation in the BBO crystal with self-phase modulation in the fused silica substrate, we efficiently generated broadband ultraviolet pulses and subsequently compress the pulses to a duration of 5 fs, achieving a peak power of 210 GW. The all-solid free-space apparatus is compact and robust, and can be scaled for higher powers, making it highly advantageous for generating intense ultraviolet pulses in the few-cycle regime. Furthermore, our method can be applied generally to achieve spectral broadening and pulse compression of ultraviolet and visible pulses through the utilization of thin nonlinear media for harmonic generation and self-phase modulation. Our work presents a significant step forward in the generation of high-power, broadband, ultrashort ultraviolet pulses, and opens up exciting possibilities for future research and applications in the realm of nonlinear physics and ultrafast science

Table4_Integrative Analysis of Gene Expression and DNA Methylation Depicting the Impact of Obesity on Breast Cancer.XLS

Obesity has been reported to be a risk factor for breast cancer, but how obesity affects breast cancer (BC) remains unclear. Although body mass index (BMI) is the most commonly used reference for obesity, it is insufficient to evaluate the obesity-related pathophysiological changes in breast tissue. The purpose of this study is to establish a DNA-methylation-based biomarker for BMI (DM-BMI) and explore the connection between obesity and BC. Using DNA methylation data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we developed DM-BMI to evaluate the degree of obesity in breast tissues. In tissues from non-BC and BC population, the DM-BMI model exhibited high accuracy in BMI prediction. In BC tissues, DM-BMI correlated with increased adipose tissue content and BC tissues with increased DM-BMI exhibited higher expression of pro-inflammatory adipokines. Next, we identified the gene expression profile relating to DM-BMI. Using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, we observed that the DM-BMI-related genes were mostly involved in the process of cancer immunity. DM-BMI is positively correlated with T cell infiltration in BC tissues. Furthermore, we observed that DM-BMI was positively correlated with immune checkpoint inhibitors (ICI) response markers in BC. Collectively, we developed a new biomarker for obesity and discovered that BC tissues from obese individuals exhibit an increased degree of immune cell infiltration, indicating that obese BC patients might be the potential beneficiaries for ICI treatment.</p