Ubiquitin-specific protease 54 regulates GLUT1-mediated aerobic glycolysis to inhibit lung adenocarcinoma progression by modifying p53 degradation.

Lung adenocarcinoma (LUAD) is one of the most prevalent types of cancer. Ubiquitination is crucial in modulating cell proliferation and aerobic glycolysis in cancer. The frequency of TP53 mutations in LUAD is approximately 50%. Currently, therapeutic targets for wild-type (WT) p53-expressing LUAD are limited. In the present study, we systemically explored the expression of ubiquitin-specific protease genes using public datasets. Then, we focused on ubiquitin-specific protease 54 (USP54), and explored its prognostic significance in LUAD patients using public datasets, analyses, and an independent cohort from our center. We found that the expression of USP54 was lower in LUAD tissues compared with that in the paracancerous tissues. Low USP54 expression levels were linked to a malignant phenotype and worse survival in patients with LUAD. The results of functional experiments revealed that up-regulation of USP54 suppressed LUAD cell proliferation in vivo and in vitro. USP54 directly interacted with p53 protein and the levels of ubiquitinated p53 were inversely related to USP54 levels, consistent with a role of USP54 in deubiquitinating p53 in p53-WT LUAD cells. Moreover, up-regulation of the USP54 expression inhibited aerobic glycolysis in LUAD cells. Importantly, we confirmed that USP54 inhibited aerobic glycolysis and the growth of tumor cells by a p53-mediated decrease in glucose transporter 1 (GLUT1) expression in p53-WT LUAD cells. Altogether, we determined a novel mechanism of survival in the p53-WT LUAD cells to endure the malnourished tumor microenvironment and provided insights into the role of USP54 in the adaptation of p53-WT LUAD cells to metabolic stress.

Biomimetic hydrogels with mesoscale collagen architecture for patient-derived tumor organoids culture.

Patient-derived tumor organoids (PDTOs) shows great potential as a preclinical model. However, the current methods for establishing PDTOs primarily focus on modulating local properties, such as sub-micrometer topographies. Nevertheless, they neglect to capture the global millimeter or intermediate mesoscale architecture that have been demonstrated to influence tumor response to therapeutic treatment and tumor progression. In this study, we present a rapid technique for generating collagen bundles with an average length of 90 ± 27 µm and a mean diameter of 5 ± 1.5 µm from tumor tissue debris that underwent mechanical agitation following enzymatic digestion. The collagen bundles were subsequently utilized for the fabrication of biomimetic hydrogels, incorporating microbial transglutaminase (mTG) crosslinked gelatin. These biomimetic hydrogels, referred to as MC-gel, were specifically designed for patient-derived tumor organoids. The lung cancer organoids cultured in MC-gel exhibited larger diameters and higher cell viability compared to those cultured in gels lacking the mesoscale collagen bundle; moreover, their irregular morphology more closely resembled that observed in vivo. The MC-gel-based lung cancer organoids effectively replicated the histology and mutational landscapes observed in the original donor patient's tumor tissue. Additionally, these lung cancer organoids showed a remarkable similarity in their gene expression and drug response across different matrices. This recently developed model holds great potential for investigating the occurrence, progression, metastasis, and management of tumors, thereby offering opportunities for personalized medicine and customized treatment options.

Two-Point Localization Algorithm of a Magnetic Target Based on Tensor Geometric Invariant.

Currently, magnetic gradient tensor-based localization methods face challenges such as significant errors in geomagnetic field estimation, susceptibility to local optima in optimization algorithms, and inefficient performance. In addressing these issues, this article propose a two-point localization method under the constraint of overlaying geometric invariants. This method initially establishes the relationship between the target position and the magnetic gradient tensor by substituting an intermediate variable for the magnetic moment. Exploiting the property of the eigenvector corresponding to the minimum absolute eigenvalue being perpendicular to the target position vector, this constraint is superimposed to formulate a nonlinear system of equations of the target's position. In the process of determining the target position, the Nara method is employed for obtaining the initial values, followed by the utilization of the Levenberg-Marquardt algorithm to derive a precise solution. Experimental validation through both simulations and experiments confirms the effectiveness of the proposed method. The results demonstrate its capability to overcome the challenges faced by a single-point localization method in the presence of some errors in geomagnetic field estimation. In comparison to traditional two-point localization methods, the proposed method exhibits the highest precision. The localization outcomes under different noise conditions underscore the robust noise resistance and resilience of the proposed method.

Squalene Epoxidase: Its Regulations and Links with Cancers.

Squalene epoxidase (SQLE) is a key enzyme in the mevalonate-cholesterol pathway that plays a critical role in cellular physiological processes. It converts squalene to 2,3-epoxysqualene and catalyzes the first oxygenation step in the pathway. Recently, intensive efforts have been made to extend the current knowledge of SQLE in cancers through functional and mechanistic studies. However, the underlying mechanisms and the role of SQLE in cancers have not been fully elucidated yet. In this review, we retrospected current knowledge of SQLE as a rate-limiting enzyme in the mevalonate-cholesterol pathway, while shedding light on its potential as a diagnostic and prognostic marker, and revealed its therapeutic values in cancers. We showed that SQLE is regulated at different levels and is involved in the crosstalk with iron-dependent cell death. Particularly, we systemically reviewed the research findings on the role of SQLE in different cancers. Finally, we discussed the therapeutic implications of SQLE inhibitors and summarized their potential clinical values. Overall, this review discussed the multifaceted mechanisms that involve SQLE to present a vivid panorama of SQLE in cancers.

Modified Broadband Ruthroff-Type Transmission Line Transformer Balun for Isolation-Enhanced Passive Mixer Design.

Generalized broadband operation facilitates multifunction or multiband highly integrated applications, such as modern transceiver systems, where ultra-wideband bidirectional passive mixers are favored to avoid a complex up/down-conversion scheme. In this paper, a modified Ruthroff-type transmission line transformer (TLT) balun is presented to enhance the isolation of the mixer from the local oscillator (LO) to the radio frequency (RF). Compared to the conventional methods, the proposed Ruthroff-type architecture adopts a combination of shunt capacitors and parallel coupled lines to improve the return loss at the LO port, thus effectively avoiding the area consumption for the diode-to-balun impedance transformation while simultaneously providing a suitable point for IF extraction. In addition, a parallel compensation technique consisting of an inductor and resistor is applied to the RF balun to significantly improve the amplitude/phase balance performance over a wide bandwidth. Benefiting from the aforementioned operations, an isolation-enhanced 8-30 GHz passive double-balanced mixer is designed as a proof-of-principle demonstration via 0.15-micrometer GaAs p-HEMT technology. It exhibits ultra-broadband performance with 7 dB average conversion loss and 50 dB LO-to-RF isolation under 15 dBm LO power. The monolithic microwave integrated circuit area is 0.96 × 1.68 mm2 including all pads.

Transcriptome Sequencing Unveils a Molecular-Stratification-Predicting Prognosis of Sarcoma Associated with Lipid Metabolism.

Sarcomas are heterogeneous connective tissue malignancies that have been historically categorized into soft tissue and bone cancers. Although multimodal therapies are implemented, many sarcoma subtypes are still difficult to treat. Lipids play vital roles in cellular activities; however, ectopic levels of lipid metabolites have an impact on tumor recurrence, metastasis, and drug resistance. Thus, precision therapies targeting lipid metabolism in sarcoma need to be explored. In this study, we performed a comprehensive analysis of molecular stratification based on lipid metabolism-associated genes (LMAGs) using both public datasets and the data of patients in our cohort and constructed a novel prognostic model consisting of squalene epoxidase (SQLE) and tumor necrosis factor (TNF). We first integrated information on gene expression profile and survival outcomes to divide TCGA sarcoma patients into high- and low-risk subgroups and further revealed the prognosis value of the metabolic signature and immune infiltration of patients in both groups, thus proposing various therapeutic recommendations for sarcoma. We observed that the low-risk sarcoma patients in the TCGA-SARC cohort were characterized by high proportions of immune cells and increased expression of immune checkpoint genes. Subsequently, this lipid metabolic signature was validated in four external independent sarcoma datasets including the CHCAMS cohort. Notably, SQLE, a rate-limiting enzyme in cholesterol biosynthesis, was identified as a potential therapeutic target for sarcoma. Knockdown of SQLE substantially inhibited cell proliferation and colony formation while promoting the apoptosis of sarcoma cells. Terbinafine, an inhibitor of SQLE, displayed similar tumor suppression capacity in vitro. The prognostic predictive model and the potential drug target SQLE might serve as valuable hints for further in-depth biological, diagnostic, and therapeutic exploration of sarcoma.

Zinc based biodegradable metals for bone repair and regeneration: Bioactivity and molecular mechanisms.

Bone fractures and critical-size bone defects are significant public health issues, and clinical treatment outcomes are closely related to the intrinsic properties of the utilized implant materials. Zinc (Zn)-based biodegradable metals (BMs) have emerged as promising bioactive materials because of their exceptional biocompatibility, appropriate mechanical properties, and controllable biodegradation. This review summarizes the state of the art in terms of Zn-based metals for bone repair and regeneration, focusing on bridging the gap between biological mechanism and required bioactivity. The molecular mechanism underlying the release of Zn ions from Zn-based BMs in the improvement of bone repair and regeneration is elucidated. By integrating clinical considerations and the specific bioactivity required for implant materials, this review summarizes the current research status of Zn-based internal fixation materials for promoting fracture healing, Zn-based scaffolds for regenerating critical-size bone defects, and Zn-based barrier membranes for reconstituting alveolar bone defects. Considering the significant progress made in the research on Zn-based BMs for potential clinical applications, the challenges and promising research directions are proposed and discussed.

E2F7 serves as a potential prognostic biomarker for lung adenocarcinoma.

E2F transcription factors (E2Fs) are a family of transcription factors critical regulators of the cell cycle, apoptosis, and differentiation, thus influencing tumorigenesis. However, the specific roles of E2Fs in lung adenocarcinoma (LUAD) remain unclear. Data from The Cancer Genome Atlas (TCGA) were used. R version. 4.0.3 and multiple databases (TIMER, cBioportal, gene expression profile interaction analysis [GEPIA], LinkedOmics, and CancerSEA) were utilized to investigate mRNA expression, mutational analysis, prognosis, clinical correlations, co-expressed gene, pathway and network, and single-cell analyses. Immunohistochemistry (IHC) confirmed that E2F transcription factor 7 (E2F7) correlated with LUAD. Among the E2Fs, E2F7 was identified by constructing a prognostic model most significantly associated with overall survival (OS) in LUAD patients. The univariate and multivariate Cox regression analyses showed that E2F7, p-T stage, and p-TNM stage were closely related to OS and progression-free survival (PFS) (P < .05) in LUAD. E2F 7/8 were also identified as significantly associated with tumor stage in the GEPIA database. Compared with paracancerous tissues, E2F7 was up-regulated in LUAD by IHC, and E2F7 might be positively correlated with larger tumors and higher TNM stages. E2F7 may primarily regulate DNA repair, damage, and cell cycle processes and thus affect LUAD tumorigenesis, invasion, and metastasis by LinkedOmics and CancerSEA. E2F7 serves as a potential prognostic biomarker for LUAD.

Regulating Lewis Acidic Sites of 1T-2H MoS2 Catalysts for Solar-Driven Photothermal Catalytic H2 Production from Lignocellulosic Biomass.

Solar-driven photothermal catalytic H2 production from lignocellulosic biomass was achieved by using 1T-2H MoS2 with tunable Lewis acidic sites as catalysts in an alkaline aqueous solution, in which the number of Lewis acidic sites derived from the exposed Mo edges of MoS2 was successfully regulated by both the formation of an edge-terminated 1T-2H phase structure and tunable layer number. Owing to the abundant Lewis acidic sites for the oxygenolysis of lignocellulosic biomass, the 1T-2H MoS2 catalyst shows high photothermal catalytic lignocellulosic biomass-to-H2 transformation performance in polar wood chips, bamboo, rice straw corncobs, and rice hull aqueous solutions, and the highest H2 generation rate and solar-to-H2 (STH) efficiency respectively achieves 3661 µmol·h-1·g-1 and 0.18% in the polar wood chip system under 300 W Xe lamp illumination. This study provides a sustainable and cost-effective method for the direct transformation of renewable lignocellulosic biomass to H2 fuel driven by solar energy.

Biocompatibility and osteogenic potential of choline phosphate chitosan-coated biodegradable Zn1Mg.

Zinc alloys have demonstrated considerable potentials as implant materials for biodegradable vascular and orthopedic applications. However, the high initial release of Zn2+ can trigger intense immune responses that impede tissue healing. To address this challenge and enhance the osteogenic capacity of zinc alloys, the surface of Zn1Mg was subjected to CO2 plasma modification (Zn1Mg-PP) followed by grafting with choline phosphate chitosan (Zn1Mg-PP-PCCs). This study aims to investigate the in vitro and in vivo biocompatibility of the surface-modified Zn1Mg. The effect of the surface modification on the inflammatory response and osteogenic repair process was investigated. Compared with unmodified Zn1Mg, the degradation rate of Zn1Mg-PP-PCCs was significantly decreased, avoiding the cytotoxicity triggered by the release of large amounts of Zn2+. Moreover, PCCs significantly enhanced the cell-material adhesion, promoted the proliferation of osteoblasts (MC3T3-E1) and upregulated the expression of key osteogenic factors in vitro. Notably, the in vivo experiments revealed that the surface modification of Zn1Mg suppressed inhibited the expression of inflammatory cytokines, promoting the secretion of anti-inflammatory factors, thereby reducing inflammation and promoting bone tissue repair. Furthermore, histological analysis of tissue sections exhibited strong integration between the material and the bone, along with well-defined new bone formation and reduced osteoclast aggregation on the surface. This was attributed to the improved immune microenvironment by PCCs, which promoted osteogenic differentiation of osteoblasts. These findings highlight that the preparation of PCCs coatings on zinc alloy surfaces effectively inhibited ion release and modulated the immune environment to promote bone tissue repair. STATEMENT OF SIGNIFICANCE: Surface modification of biodegradable Zn alloys facilitates the suppression of intense immune responses caused by excessive ion release concentrations from implants. We modified the surface of Zn1Mg with choline phosphate chitosan (PCCs) and investigated the effects of surface modification on the inflammatory response and osteogenic repair process. In vitro results showed that the PCCs coating effectively reduced the degradation rate of Zn1Mg to avoid cytotoxicity caused by high Zn2+ concentration, favoring the proliferation of osteoblasts. In addition, in vivo results indicated that Zn1Mg-PP-PCCs attenuated inflammation to promote bone repair by modulating the release of inflammation-related factors. The surface-modified Zn1Mg implants demonstrated strong osseointegration, indicating that the PCCs coating effectively modulated the immune microenvironment and promoted bone healing.

CTRP6 protects against ferroptosis to drive lung cancer progression and metastasis by destabilizing SOCS2 and augmenting the xCT/GPX4 pathway.

Lung cancer is a highly heterogeneous malignancy, and despite the rapid development of chemotherapy and radiotherapy, acquired drug resistance and tumor progression still occur. Thus, it is urgent to identify novel therapeutic targets. Our research aims to screen novel biomarkers associated with the prognosis of lung carcinoma patients and explore the potential regulatory mechanisms. We obtained RNA sequencing (RNA-seq) data of lung cancer patients from public databases. Clinical signature analysis, weighted gene coexpression network analysis (WGCNA) and the random forest algorithm showed that C1q/tumor necrosis factor-related protein-6 (CTRP6) is a core gene related to lung cancer prognosis, and it was determined to promote tumor proliferation and metastasis both in vivo and in vitro. Mechanistically, silencing CTRP6 was determined to promote xCT/GPX4-involved ferroptosis through functional assays related to lipid peroxidation, Fe2+ concentration and mitochondrial ultrastructure. By performing interactive proteomics analyses in lung tumor cells, we identified the interaction between CTRP6 and suppressor of cytokine signaling 2 (SOCS2) leading to SOCS2 ubiquitination degradation, subsequently enhancing the downstream xCT/GPX4 signaling pathway. Moreover, significant correlations between CTRP6-mediated SOCS2 and ferroptosis were revealed in mouse models and clinical specimens of lung cancer. As inducing ferroptosis has been gradually regarded as an alternative strategy to treat tumors, targeting CTRP6-mediated ferroptosis could be a potential strategy for lung cancer therapy.

USP4 promotes the proliferation, migration, and invasion of esophageal squamous cell carcinoma by targeting TAK1.

Ubiquitin-specific protease 4 (USP4) represents a potential oncogene involved in various human cancers. Nevertheless, the biological roles and precise mechanism of USP4 in esophageal squamous cell carcinoma (ESCC) progression are not understood. Here, USP4 expression was found to be markedly upregulated in ESCC tumor tissues and cells. Loss- and gain-of-function assays suggested that USP4 silencing inhibited ESCC cell proliferation, migration, and invasion, while USP4 overexpression promoted these behaviors. Consistently, USP4 silencing repressed tumor growth and metastasis in an ESCC nude mouse model in vivo. As a target molecule of USP4, transforming growth factor-ß-activated kinase 1 (TAK1) also showed high expression in ESCC. Moreover, we observed that USP4 specifically interacted with TAK1 and stabilized TAK1 protein levels via deubiquitination in ESCC cells. Importantly, USP4 promotes ESCC proliferation, migration, and invasion via the MEK/ERK signaling pathway and can be inhibited by U0126. Neutral red (NR), an inhibitor of USP4 can suppress ESCC progression in vitro and in vivo. Overall, this study revealed that USP4/TAK1 plays crucial roles in ESCC progression by modulating proliferation, migration, and invasion, and USP4 might be a potential therapeutic target in ESCC.

Development and clinical validation of a microfluidic-based platform for CTC enrichment and downstream molecular analysis.

Background: Although many CTC isolation and detection methods can provide information on cancer cell counts, downstream gene and protein analysis remain incomplete. Therefore, it is crucial to develop a technology that can provide comprehensive information on both the number and profile of CTC. Methods: In this study, we developed a novel microfluidics-based CTC separation and enrichment platform that provided detailed information about CTC. Results: This platform exhibits exceptional functionality, achieving high rates of CTC recovery (87.1%) and purification (∼4 log depletion of WBCs), as well as accurate detection (95.10%), providing intact and viable CTCs for downstream analysis. This platform enables successful separation and enrichment of CTCs from a 4 mL whole-blood sample within 15 minutes. Additionally, CTC subtypes, selected protein expression levels on the CTC surface, and target mutations in selected genes can be directly analyzed for clinical utility using immunofluorescence and real-time polymerase chain reaction, and the detected PD-L1 expression in CTCs is consistent with immunohistochemical assay results. Conclusion: The microfluidic-based CTC enrichment platform and downstream molecular analysis together provide a possible alternative to tissue biopsy for precision cancer management, especially for patients whose tissue biopsies are unavailable.

Uncovering Diverse Mechanistic Spreading Pathways in Disease Progression of Alzheimer's Disease.

Background: The AT[N] research framework focuses on three major biomarkers in Alzheimer's disease (AD): amyloid-ß deposition (A), pathologic tau (T), and neurodegeneration [N]. Objective: We hypothesize that the diverse mechanisms such as A⟶T and A⟶[N] pathways from one brain region to others, may underlie the wide variation in clinical symptoms. We aim to uncover the causal-like effect of regional AT[N] biomarkers on cognitive decline as well as the interaction with non-modifiable risk factors such as age and APOE4. Methods: We apply multi-variate statistical inference to uncover all possible mechanistic spreading pathways through which the aggregation of an upstream biomarker (e.g., increased amyloid level) in a particular brain region indirectly impacts cognitive decline, via the cascade build-up of a downstream biomarker (e.g., reduced metabolism level) in another brain region. Furthermore, we investigate the survival time for each identified region-to-region pathological pathway toward the AD onset. Results: We have identified a collection of critical brain regions on which the amyloid burdens exert an indirect effect on the decline in memory and executive function (EF) domain, being mediated by the reduction of metabolism level at other brain regions. APOE4 status has been found not only involved in many A⟶N mechanistic pathways but also significantly contributes to the risk of developing AD. Conclusion: Our major findings include 1) the region-to-region A⟶N⟶MEM and A⟶N⟶MEM pathways exhibit distinct spatial patterns; 2) APOE4 is significantly associated with both direct and indirect effects on the cognitive decline while sex difference has not been identified in the mediation analysis.

Native frustrated Lewis pairs on core-shell In@InOxHy enhances CO2-to-formate conversion.

Strategies to efficiently activate CO2 by strongly inhibiting the competitive hydrogen evolution reaction process are highly desired for practical applications of the electrochemical CO2 reduction technique. Here, we assembled a core-shell In@InOxHy architecture on carbon black by one-step reduction of NaBH4 as a CO2-to-formate catalyst with high selectivity. The stable CO2-to-formate reaction originates from the creation of steritic frustrated Lewis pairs (FLPs) on the InOxHy shell with In-OVs (OVs, oxygen vacancies) Lewis acid, and In-OH Lewis base. During CO2 reduction, the electrochemically stable FLPs are capable of first capturing and stabilizing protons to protonate FLPs to In-H Lewis acid and In-OH2 Lewis base due to its strong steric electrostatic field; then, CO2 is captured and activated by the protonated FLPs to selectively produce formate. Our results demonstrated that FLPs can be created on the surface of oxyphilic single-metal catalysts efficient in accelerating CO2 reduction with high selectivity.

Development and validation of web-based dynamic nomograms predictive of disease-free and overall survival in patients who underwent pneumonectomy for primary lung cancer.

Background: The tumour-node-metastasis (TNM) staging system is insufficient to precisely distinguish the long-term survival of patients who underwent pneumonectomy for primary lung cancer. Therefore, this study sought to identify determinants of disease-free (DFS) and overall survival (OS) for incorporation into web-based dynamic nomograms. Methods: The clinicopathological variables, surgical methods and follow-up information of 1,261 consecutive patients who underwent pneumonectomy for primary lung cancer between January 2008 and December 2018 at Sun Yat-sen University Cancer Center were collected. Nomograms for predicting DFS and OS were built based on the significantly independent predictors identified in the training cohort (n = 1,009) and then were tested on the validation cohort (n = 252). The concordance index (C-index) and time-independent area under the receiver-operator characteristic curve (AUC) assessed the nomogram's discrimination accuracy. Decision curve analysis (DCA) was applied to evaluate the clinical utility. Results: During a median follow-up time of 40.5 months, disease recurrence and death were observed in 446 (35.4%) and 665 (52.7%) patients in the whole cohort, respectively. In the training cohort, a higher C-reactive protein to albumin ratio, intrapericardial pulmonary artery ligation, lymph node metastasis, and adjuvant therapy were significantly correlated with a higher risk for disease recurrence; similarly, the independent predictors for worse OS were intrapericardial pulmonary artery and vein ligation, higher T stage, lymph node metastasis, and no adjuvant therapy. In the validation cohort, the integrated DFS and OS nomograms showed well-fitted calibration curves and yielded good discrimination powers with C-index of 0.667 (95% confidence intervals CIs [0.610-0.724]) and 0.697 (95% CIs [0.649-0.745]), respectively. Moreover, the AUCs for 1-year, 3-year, and 5-year DFS were 0.655, 0.726, and 0.735, respectively, and those for 3-year, 5-year, and 10-year OS were 0.741, 0.765, and 0.709, respectively. DCA demonstrated that our nomograms could bring more net benefit than the TNM staging system. Conclusions: Although pneumonectomy for primary lung cancer has brought encouraging long-term outcomes, the constructed prediction models could assist in precisely identifying patients at high risk and developing personalized treatment strategies to further improve survival.

Novel Approach for Rate Transient Analysis of Fractured Wells from Carbonate Reservoirs with Heterogeneous Natural Fractures.

This paper developed a new methodology for rate transient analysis of fractured wells in carbonate reservoirs. Both the heterogeneity and dual-permeability flow behavior are incorporated into the proposed model, and the fractured carbonate reservoir was simulated with a two-zone composite model. In each zone, a traditional dual-porosity model was applied to describe the characteristics of the natural fractures and matrix. With the Laplace transform, we derived the solution of the mathematical model and plotted new type curves for transient rate decline analysis. Then, the flow regimes were divided and analyzed based on the new type curves. The influences of several critical parameters on transient rate response were also examined. A field case was studied further to demonstrate the precision and application of the proposed method. The results show that the new type curves are mainly composed of eight flow stages. The difference in physical properties (k 2,1, η2,1) between the two zones significantly impacts the transition and boundary-dominated flow regimes. When the values of k 2,1 and η2,1 are smaller, the derivative curve of the transition flow stage will move down, and the duration of this stage on the derivative curve is longer, while the duration of the boundary dominant flow stage will decrease. The dimensionless radial radius of the inner zone (r 1D) can significantly influence the transition flow regime. When r 1D is larger, the production rate and its derivative curve of the transition flow stage will move up, and the duration of this stage will be longer. The results also show that the proposed methodology can effectively fit the field production data. This method can be applied in well productivity evaluation for fractured carbonate reservoirs.

High expression of PPFIA1 in human esophageal squamous cell carcinoma correlates with tumor metastasis and poor prognosis.

BACKGROUND: PTPRF interacting protein alpha 1 (PPFIA1) is reportedly related to the occurrence and progression of several kinds of malignancies. However, its role in esophageal squamous cell carcinoma (ESCC) is unclear. This current study investigated the prognostic significance and biological functions of PPFIA1 in ESCC. METHODS: Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), and Gene Expression Omnibus (GEO) were used to investigate PPFIA1 expression in esophageal cancer. The relationship between PPFIA1 expression and clinicopathological characteristics and patient survival was evaluated in GSE53625 dataset, and verified in the cDNA array based on qRT-PCR and tissue microarray (TMA) dataset based on immunohistochemistry. The impact of PPFIA1 on the migration and invasion of cancer cells were investigated by wound-healing and transwell assays, respectively. RESULTS: The expression of PPFIA1 was obviously increased in ESCC tissues versus adjacent esophageal tissues according to online database analyses (all P < 0.05). High PPFIA1 expression was closely related to several clinicopathological characteristics, including tumor location, histological grade, tumor invasion depth, lymph node metastasis, and tumor-node-metastasis (TNM) stage. High PPFIA1 expression was related to worse outcomes and was identified as an independent prognostic factor of overall survival in ESCC patients (GSE53625 dataset, P = 0.019; cDNA array dataset, P < 0.001; TMA dataset, P = 0.039). Downregulation of PPFIA1 expression can significantly reduce the migration and invasion ability of ESCC cells. CONCLUSION: PPFIA1 is related to the migration and invasion of ESCC cells, and can be used as a potential biomarker to evaluate the prognosis of ESCC patients.

Flexible Film Bulk Acoustic Resonator Based on Low-Porosity ß-Phase P(VDF-TrFE) Film for Human Vital Signs Monitoring.

P(VDF-TrFE) is a promising material for flexible acoustic devices owing to its good piezoelectric performance and excellent stretchability. However, the high density of internal pores and large surface roughness of the conventional P(VDF-TrFE) results in a high propagation attenuation for acoustic waves, which limits its use in flexible acoustic devices. In this paper, a novel method based on two-step annealing is proposed to effectively remove the pores inside the P(VDF-TrFE) film and reduce its surface roughness. The obtained P(VDF-TrFE) film possesses excellent characteristics, including a high breakdown strength of >300 kV/mm, a high-purity ß-phase content of more than 80%, and high piezoelectric coefficients (d33) of 42 pm/V. Based on the low-porosity ß-phase P(VDF-TrFE) film, we fabricated flexible film bulk acoustic resonators (FBARs) which exhibit high sharp resonance peaks. The pressure sensor was made by sandwiching the FBARs with two PDMS microneedle patches. Heartbeat and respiration rate monitoring were achieved using the pressure sensor. This work demonstrates the feasibility of high-performance flexible piezoelectric acoustic resonators based on low-porosity P(VDF-TrFE) films, which could see wider applications in the wearable sensors for both physical and chemical sensing.

Synthesis and Characterization of an Novel Intercalated Polyacrylamide/Clay Nanocomposite.

Solving the problem of the low temperature and low salt resistances of conventional polyacrylamide and the high cost of functional monomers, and thus, introducing it to the interlayer space provided by a layered structure for polymer modification, is a promising option. In this study, montmorillonite was used as the inorganic clay mineral, and an intercalated polyacrylamide/clay nanocomposite was synthesized via in situ intercalation polymerization. The optimal synthesis conditions were a clay content of 10.7%, preparation temperature of 11 °C, initiator concentration of 2.5 × 10-4 mol/L, and chain extender concentration of 5%. The IR results showed that the polymer was successfully introduced to the nanocomposite. The synthesized intercalated polyacrylamide/clay nanocomposite exhibited a better thickening effect, good viscoelasticity, and better salt resistance and thermal stability than polyacrylamide. In addition, the thickening capacity and thermal stability were superior to the salt-resistant polymer, with a 16.0% higher thickening viscosity and a 15.1% higher viscosity retention rate at 85 °C for 60 d. The intercalated polyacrylamide/clay nanocomposite further expanded the application of polyacrylamide in petroleum exploitation.