Luengberg4431

A simple cryo-transfer method to fabricate ultrathin, stretchable, and conformal epidermal electrodes based on a combination of silver nanowires (AgNWs) network and elastomeric polymers is developed. This method can temporarily enable the soft elastomers with much higher elastic modulus and dimensional contraction through exploiting their glass-transition behaviors. During this process, a much higher Von Mises stress can be loaded on AgNWs than usual, and the generated strong grip force can facilitate the complete transfer of AgNWs. Afterward, the thawed AgNWs and elastomer composites quickly recover to their soft state at room temperature. The obtained ultrathin and soft electrode with a thickness of 8.4 µm and transmittance of 90.8% at a sheet resistance of 13.2 Ω sq-1 can tolerate a stretching strain of 70% and 50 000 repeated bending cycles, which meets rigorous requirements of epidermal applications. The as-prepared epidermal electrodes are effective and comfortable for electrophysiological signal monitoring, and while showing excellent performance exceeding the commercialized gel electrodes.Background Prostate cancer (PCa) is generally detected by prostate-specific antigen (PSA) as one of the most widely applied tumor markers over decades for its high sensitivity. Nevertheless, it causes overtreatment or an unnecessary biopsy because of its limited specificity. Prostate cancer-associated ncRNA transcript 1 (PCAT1), the newly identified long non-coding RNA (lncRNA) has been reported to associate with the progress of prostate cancer. In vitro studies proposed that PCAT-1 may be an appealing candidate for diagnostic accuracy improvement regard to its notable overexpression in prostate cancer cells. The purpose of the present study was to evaluate the diagnostic potential of the plasma PCAT1 expression levels in prostate cancer patients in comparison to benign prostatic hyperplasia (BPH) patients and healthy controls. Methods The plasma lncRNA PCAT1 level was measured by real-time quantitative reverse transcription PCR in 40 men newly diagnosed with PCa, 20 patients with BPH and 20 healthy subjects. The results were analyzed statistically by SPSS software 25. Results The expression of PCAT1 was significantly higher in healthy subjects compared to BPH patients (P=0.03). The diagnostic accuracy of the plasma lncRNA PCAT-1 for discrimination of the healthy subjects than BPH patients was reasonable (AUC=0.799; sensitivity=71%; specificity=74%; NPV=74%; PPV=71%). Conclusions It seems that the plasma levels of PCAT1 expression have reasonable diagnostic accuracy for the discrimination of healthy individuals than BPH. While no significant difference of PCAT1 expression levels in comparisons between prostate cancer group with BPH and normal groups was observed.Adipose tissue (AT) has a dynamic extracellular matrix (ECM) surrounding adipocytes that allows for remodeling during metabolic fluctuations. During the progression of obesity, AT has increased ECM deposition, stiffening, and remodeling, resulting in a pro-fibrotic dysfunctional state. Here, the incorporation of ethylene glycol-bis-succinic acid N-hydroxysuccinimide ester (PEGDS) allows for control over 3D collagen hydrogel stiffness and architecture to investigate its influence on adipocyte metabolic and fibrotic function. Upon stiffening and altering ECM architecture, adipocytes did not alter their expression of key adipokines, leptin, and adiponectin. However, they do increase actin cytoskeletal fiber formation, pro-fibrotic gene expression, ECM deposition, and remodeling within a stiffer, 3D collagen hydrogel. For example, COL6A3 gene expression is upregulated approximately twofold, resulting in increased deposition of pericellular collagen VI alpha 3 surrounding adipocytes. Furthermore, inhibition of actin contractility results in a reversal of pro-fibrotic gene expression and ECM deposition, indicating that adipocytes are mediating mechanical cues through actin cytoskeletal networks. This study demonstrates that ECM stiffness and architecture plays a critical regulatory role in adipocyte fibrotic function and contributes to the overall pro-fibrotic dysfunctional state of AT during the progression of obesity and AT fibrosis.Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death primarily due to the lack of effective targeted therapies. Despite the distinct morphological and phenotypic patterns of HCC, treatment strategies are restricted to relatively homogeneous therapies, including multitargeted tyrosine kinase inhibitors and immune checkpoint inhibitors. Therefore, more effective therapy options are needed to target dysregulated metabolic and molecular pathways in HCC. Integrative genomic profiling of HCC patients provides insight into the most frequently mutated genes and molecular targets, including telomerase reverse transcriptase, the TP53 gene, and the Wnt/β-catenin signaling pathway oncogene (CTNNB1). Moreover, emerging techniques, such as genome-scale metabolic models may elucidate the underlying cancer-specific metabolism, which allows for the discovery of potential drug targets and identification of biomarkers. De novo lipogenesis has been revealed as consistently upregulated since it is required for cell proliferation in all HCC patients. The metabolic network-driven stratification of HCC patients in terms of redox responses, utilization of metabolites, and subtype-specific pathways may have clinical implications to drive the development of personalized medicine. In this review, the current and emerging therapeutic targets in light of molecular approaches and metabolic network-based strategies are summarized, prompting effective treatment of HCC patients.Ex vivo culture of viable circulating tumor cells (CTCs) from individual patients has recently become an emerging liquid biopsy technology to investigate drug sensitivity and genomic analysis in cancer. However, it remains challenging to retrieve the CTCs with high viability and purity from cancer patients' blood using a rapid process. Here, a triple selection strategy that combines immunonegative enrichment, density gradient, and microfluidic-based size-exclusion methods is developed for in situ drug sensitivity testing. this website The CTC isolation chip consists of 4 independent microchannels that can evenly distribute the captured CTCs, allowing for independent in situ analysis event. The cancer cells are retrieved within 5 min with high viability (>95%), captured efficiency (78%), and high purity (99%) from 7.5 mL of blood cell mixed samples. Furthermore, the CTCs can be isolated from prostate cancer patients' blood samples and verified in situ using cancer-specific markers within 1.5 h, demonstrating the possibility to be applied to clinical practice.