Microstructural evolution of Cu–Sn–Ni compounds in full intermetallic micro-joint and in situ micro-bending test

This study focuses on the microstructural evolution process of Cu–Sn–Ni intermetallic compounds (IMCs) interlayer in the micro-joints, formed from the initial Ni/Sn (1.5 µm)/Cu structure through transient liquid phase (TLP) soldering. Under the bonding temperature of 240 °C, the micro-joints evolve into Ni/(Cu, Ni)6Sn5/(Cu, Ni)3Sn/Cu structure, where the interfacial reactions on Cu/Sn and Sn/Ni are suppressed by the atoms diffusing from the opposite side. The thickness of (Cu, Ni)3Sn layer on plated Cu layer still increases with the prolonged dwell time. When the bonding temperature was elevated to 290 °C, the phase transformation of (Cu, Ni)6Sn5 into (Cu, Ni)3Sn has been accelerated, thus the majority of IMCs interlayer is constituted with (Cu, Ni)3Sn. However, a small amount of Ni-rich (Cu, Ni)6Sn5 phases still remain near the Ni substrate and some of them close to the center-line of IMCs interlayer. The state between (Cu, Ni)6Sn5 and the adjacent (Cu, Ni)3Sn tends to reach equilibrium in Ni content based on the observation from Transmission Electron Microscope (TEM). In addition, the Cu–Sn–Ni IMCs micro-cantilevers were fabricated from these micro-joints using Focus Ion Beam (FIB) for the in situ micro-bending test, the results indicate a high ultimate tensile strength as well as the brittle fracture in the inter- and transgranular modes

Table1_A novel cuproptosis-related lncRNAs signature predicts prognostic and immune of bladder urothelial carcinoma.DOCX

Bladder Urothelial Carcinoma (BLCA) remains the most common urinary system tumor, and its prognosis is poor. Cuproptosis is a recently discovered novel cell death involved in the development of tumor cells. However, the use of cuproptosis to predict the prognosis and immunity of Bladder Urothelial Carcinoma remains largely unclear, and this study was designed to verify cuproptosis-related long non-coding RNAs (lncRNAs) to estimate the prognosis and immunity of Bladder Urothelial Carcinoma. In our study, we first defined the expression of cuproptosis-related genes (CRGs) in BLCA, and 10 CRGs were up- or downregulated. We then constructed a co-expression network of cuproptosis-related mRNA and long non-coding RNAs using RNA sequence data from The Cancer Genome Atlas Bladder Urothelial Carcinoma (TCGA-BLCA), clinical features and mutation data from BLCA patients to obtain long non-coding RNAs by Pearson analysis. Afterward, univariate and multivariate COX analysis identified 21 long non-coding RNAs as independent prognostic factors and used these long non-coding RNAs to construct a prognostic model. Then, survival analysis, principal component analysis (PCA), immunoassay, and comparison of tumor mutation frequencies were performed to verify the accuracy of the constructed model, and GO and KEGG functional enrichment analysis was used to verify further whether cuproptosis-related long non-coding RNAs were associated with biological pathways. The results showed that the model constructed with cuproptosis-related long non-coding RNAs could effectively evaluate the prognosis of BLCA, and these long non-coding RNAs were involved in numerous biological pathways. Finally, we performed immune infiltration, immune checkpoint and drug sensitivity analyses on four genes (TTN, ARID1A, KDM6A, RB1) that were highly mutated in the high-risk group to evaluate the immune association of risk genes with BLCA. In conclusion, the cuproptosis-related lncRNA markers constructed in this study have evaluation value for prognosis and immunity in BLCA, which can provide a certain reference for the treatment and immunity of BLCA.</p

Additional file 1: of Continuous weeklong measurements of indoor particle levels in a Minnesota Tribal Casino Resort

Supplementary dataset. (XLSX 739 kb

Regulated Dielectric Loss of Polymer Composites from Coating Carbon Nanotubes with a Cross-Linked Silsesquioxane Shell through Free-Radical Polymerization

We report a synthetic strategy for coating multiwalled carbon nanotubes (MWCNTs) with cross-linked octa-methacrylate-polyhedral oligomeric silsesquioxane (MA-POSS) by direct, in situ free-radical polymerization in a controlled manner. This strategy resulted in a core–shell structure with an MWCNT center. The shell thickness could be varied from ∼7 nm to 40 nm by choosing different initiators, solvents, and weight ratios of MWCNT and octa-MA-POSS. Coated MWCNT hybrids had controlled electrical performance depending on the coating layer thickness and were well-dispersed in the polymer matrix. POSS-coated MWCNTs were compounded with poly­(vinylidene fluoride) to obtain a composite with high dielectric permittivity and low dielectric loss

Image1_Prognostic and immune correlation evaluation of a novel cuproptosis-related genes signature in hepatocellular carcinoma.JPEG

Hepatocellular carcinoma (HCC) is one of the world’s malignant tumors with high morbidity and mortality. Cuproptosis is a novel form of cell death. However, the prognostic evaluation and immune relevance of cuproptosis-related genes (CRGs) in HCC are largely unknown. In our study, we constructed a prognostic model of CRGs in HCC and performed immune infiltration, functional analysis, immune checkpoint and drug sensitivity analysis. Systematically elaborated the prognostic and immune correlation of CRGs in HCC. The results showed that 15 CRGs were up-regulated or down-regulated in HCC, and the mutation frequency of CRGs reached 10.33% in HCC, with CDKN2A having the highest mutation frequency. These 19 CRGs were mainly involved in the mitochondrion, immune response and metabolic pathways. Five selected genes (CDKN2A, DLAT, DLST, GLS, PDHA1) were involved in constructing a prognostic CRGs model that enables the overall survival in HCC patients to be predicted with moderate to high accuracy. Prognostic CRGs, especially CDKN2A, the independent factor of HCC prognosis, may be closely associated with immune-cell infiltration, tumor mutation burden (TMB), microsatellite instability(MSI), and immune checkpoints. CD274, CTLA4, LAG3, PDCD1, PDCD1LG2 and SIGLEC15 may be identified as potential therapeutic targets and CD274 correlated highly with prognostic genes. Quantitative Real-Time PCR (qRT-PCR) and immunohistochemical were performed to validate the mRNA and protein expression levels of CDKN2A in adjacent normal tissues and HCC tissues, and the results were consistent with gene difference analysis. In conclusion, CRGs, especially CDKN2A, may serve as potential prognostic predictors in HCC patients and provide novel insights into cancer therapy.</p

Table1_Prognostic and immune correlation evaluation of a novel cuproptosis-related genes signature in hepatocellular carcinoma.DOCX

Hepatocellular carcinoma (HCC) is one of the world’s malignant tumors with high morbidity and mortality. Cuproptosis is a novel form of cell death. However, the prognostic evaluation and immune relevance of cuproptosis-related genes (CRGs) in HCC are largely unknown. In our study, we constructed a prognostic model of CRGs in HCC and performed immune infiltration, functional analysis, immune checkpoint and drug sensitivity analysis. Systematically elaborated the prognostic and immune correlation of CRGs in HCC. The results showed that 15 CRGs were up-regulated or down-regulated in HCC, and the mutation frequency of CRGs reached 10.33% in HCC, with CDKN2A having the highest mutation frequency. These 19 CRGs were mainly involved in the mitochondrion, immune response and metabolic pathways. Five selected genes (CDKN2A, DLAT, DLST, GLS, PDHA1) were involved in constructing a prognostic CRGs model that enables the overall survival in HCC patients to be predicted with moderate to high accuracy. Prognostic CRGs, especially CDKN2A, the independent factor of HCC prognosis, may be closely associated with immune-cell infiltration, tumor mutation burden (TMB), microsatellite instability(MSI), and immune checkpoints. CD274, CTLA4, LAG3, PDCD1, PDCD1LG2 and SIGLEC15 may be identified as potential therapeutic targets and CD274 correlated highly with prognostic genes. Quantitative Real-Time PCR (qRT-PCR) and immunohistochemical were performed to validate the mRNA and protein expression levels of CDKN2A in adjacent normal tissues and HCC tissues, and the results were consistent with gene difference analysis. In conclusion, CRGs, especially CDKN2A, may serve as potential prognostic predictors in HCC patients and provide novel insights into cancer therapy.</p

Additional file 1: Table S1. of Body condition score prior to parturition is associated with plasma and adipose tissue biomarkers of lipid metabolism and inflammation in Holstein cows

Gene accession number, symbol, and forward and reverse sequences. Table S2. Sequencing results obtained from PCR products. Table S3. qPCR performance of genes measured in subcutaneous adipose tissue. (DOCX 19 kb

Interplay of Charge and Aromaticity Upon Chemical Reduction of <i>p</i>‑Quinquephenyl with Alkali Metals

Chemical reduction study of a paraphenylene comprising five para-connected aromatic rings, namely, p-quinquephenyl (C30H22, 1), with alkali metals in THF revealed a facile formation of the doubly reduced anion, 12–, which was crystallized with different alkali metal counterions. Several products were characterized using single-crystal X-ray diffraction and spectroscopic methods. The use of different alkali metals allowed tuning of metal binding in the resulting crystalline products. The consequences of electron addition and metal complexation on the core of p-quinquephenyl were investigated with the help of computational methods. Most notably, reduction results in a shift from locally aromatic to quinoidal character of 12–, which is mitigated by complexation to the alkali metal cations

Western blot analysis to validate the reactive proteins.

<p>Klebsiella pneumonia from Klebsiella pneumonia bacteremia patients with (<b>A</b>) leukopenia and (<b>B</b>) leukocytosis were respectively examined by Western blot analysis to validate the reactive proteins ef-tu. Note the higher expression levels of ef-tu in patients with leukopenia caused by Klebsiella pneumonia.</p

How Does Domain Replacement Affect Fibril Formation of the Rabbit/Human Prion Proteins

<div><p>Background</p><p>It is known that <i>in vivo</i> human prion protein (PrP) have the tendency to form fibril deposits and are associated with infectious fatal prion diseases, while the rabbit PrP does not readily form fibrils and is unlikely to cause prion diseases. Although we have previously demonstrated that amyloid fibrils formed by the rabbit PrP and the human PrP have different secondary structures and macromolecular crowding has different effects on fibril formation of the rabbit/human PrPs, we do not know which domains of PrPs cause such differences. In this study, we have constructed two PrP chimeras, rabbit chimera and human chimera, and investigated how domain replacement affects fibril formation of the rabbit/human PrPs.</p><p>Methodology/Principal Findings</p><p>As revealed by thioflavin T binding assays and Sarkosyl-soluble SDS-PAGE, the presence of a strong crowding agent dramatically promotes fibril formation of both chimeras. As evidenced by circular dichroism, Fourier transform infrared spectroscopy, and proteinase K digestion assays, amyloid fibrils formed by human chimera have secondary structures and proteinase K-resistant features similar to those formed by the human PrP. However, amyloid fibrils formed by rabbit chimera have proteinase K-resistant features and secondary structures in crowded physiological environments different from those formed by the rabbit PrP, and secondary structures in dilute solutions similar to the rabbit PrP. The results from transmission electron microscopy show that macromolecular crowding caused human chimera but not rabbit chimera to form short fibrils and non-fibrillar particles.</p><p>Conclusions/Significance</p><p>We demonstrate for the first time that the domains beyond PrP-H2H3 (β-strand 1, α-helix 1, and β-strand 2) have a remarkable effect on fibrillization of the rabbit PrP but almost no effect on the human PrP. Our findings can help to explain why amyloid fibrils formed by the rabbit PrP and the human PrP have different secondary structures and why macromolecular crowding has different effects on fibrillization of PrPs from different species.</p></div