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In this work, we developed off-plane quartz-enhanced photoacoustic spectroscopy (OP-QEPAS). In the OP-QEPAS the light beam went neither through the prong spacing of the quartz tuning fork (QTF) nor in the QTF plane. The light beam is in parallel with the QTF with an optimal distance, resulting in low background noise. A radial-cavity (RC) resonator was coupled with the QTF to enhance the photoacoustic signal by the radial resonance mode. By offsetting both the QTF and the laser position from the central axis, we enhance the effect of the acoustic radial resonance and prevent the noise generated by direct laser irradiation of the QTF. Compared to IP-QEPAS based on a bare QTF, the developed OP-QEPAS with a RC resonator showed a >10× signal-to-noise ratio (SNR) enhancement. The OP-QEPAS system has great advantages in the use of light emitting devices (LEDs), long-wavelength laser sources such as mid-infrared quantum cascade lasers, and terahertz sources. When employing a LED as the excitation source, the noise level was suppressed by â¼2 orders of magnitude. Furthermore, the radial and longitudinal resonance modes can be combined to further improve the sensor performance.
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Invasive pituitary neuroendocrine tumors (PitNETs) are the most prevalent types of intracranial and neuroendocrine tumors. Their aggressive growth and difficulty in complete resection result in a high recurrence rate. Cystine transporter solute carrier family 7 member 11 (SLC7A11) is overexpressed in various cancers, which contributes to tumor growth, progression, and metastasis by promoting cystine uptake and glutathione biosynthesis. We identified SLC7A11 as an invasive biomarker based on three Gene Expression Omnibus cohorts. This study aimed to investigate the role of SLC7A11 in invasive PitNETs. Cell proliferation was assessed using CCK-8 and colony formation assays, while cell apoptosis was estimated with flow cytometry. Wound healing assays and transwell assays were utilized to evaluate migration and invasion ability. Our findings demonstrated that SLC7A11 was markedly upregulated in invasive PitNETs, and was associated with the invasiveness of PitNETs. Knockdown of SLC7A11 could largely suppress tumor cell proliferation, migration, and invasion, while inducing apoptosis. Furthermore, SLC7A11 depletion was implicated in regulating epithelial-mesenchymal transition and inactivating the PI3K/AKT signaling pathway. These insights suggest SLC7A11 as a potential therapeutic target for invasive PitNETs.
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In the present study, an environmentally friendly oil- and water-resistant paper was developed using a holo-lignocellulosic nanofibril (LCNF)-based composite coating. The LCNF was prepared from wheat straw using a biomechanical method. Characterizations of oil- and water-resistant coated paper and the effect of LCNF content on the performance of the coated paper were confirmed by combining contact angle analysis, Cobb 300s, and mechanical performance tests. The results show that the barrier performance and mechanical strength of the coated paper were greatly improved with the increase of LCNF content. The contact angle of oil and water of coated paper containing 50% LCNF were 69° and 78°, respectively, while the contact angle of oil and water of the base paper were only 30° and 20°, respectively. Cobb 300s values reduced from 110 g/m2 to 30 g/m2 when the LCNF content increased from 50% to 90%. Moreover, under the coating amount of 20 g/m2, the tensile strength of the coating paper was 0.980 KN/m, an increase of 10.11% compared with the base paper. The bursting strength reached 701.930 KPa, which was 10.75% higher than the base paper. In short, it is feasible to prepare LCNF from wheat straw, and apply it to produce water-proof and oil-proof paper. The water-proof and oil-proof paper developed in this study not only offers a novel approach to addressing white pollution but also presents a new research avenue for exploring the potential applications of agricultural waste.
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BACKGROUND: Copper-dependent controlled cell death (cuproptosis) is a novel cell death modality that is distinct from known cell death mechanisms. Nonetheless, the potential role of the cuproptosis regulator in tumour microenvironment (TME) of GBM remains unknown. METHODS: Based on 13 widely recognised cuproptosis regulators, the cuproptosis regulation patterns and the biological characteristics of each pattern were comprehensively assessed in GBMs. Machine learning strategies were used to construct a CupScore to quantify the cuproptosis regulation patterns of individual tumours. A PPI network was constructed to predict core-associated genes of cuproptosis regulators. The function of the novel cuproptosis regulators SLC30A7 was examined by in vitro and in vivo experiment. RESULTS: We identified three distinct cuproptosis regulation patterns, including immune activation, metabolic activation, and immunometabolic double deletion patterns. The CupScore was shown to predict the abundance of tumour inflammation, molecular subtype, stromal activity, gene variation, signalling pathways, and patient prognosis. The low CupScore subtype was characterised by immune activation, isocitrate dehydrogenase mutations, sensitivity to chemotherapy, and clinical benefits. The high CupScore subtype was characterised by activation of the stroma and metabolism and poor survival. Novel cuproptosis regulator SLC30A7 knockdown inhibited the cuproptosi via JAK2/STAT3/ATP7A pathway in GBM. CONCLUSION: Cuproptosis regulators have been shown to play a vital role in TME complexity. Constructing CupScores were trained to evaluate the regulation patterns of cuproptosis in individual tumours. The novel cuproptosis-related genes SLC30A7 was involved in regulation the tumorigenicity of GBM cell via JAK2/STAT3/ATP7A pathway in vitro and in vivo.