Neoadjuvant therapy for non-small cell lung cancer and esophageal cancer.

As the major malignant tumors in the chest, non-small cell lung cancer (NSCLC) and esophageal cancer (EC) bring huge health burden to human beings worldwide. Currently, surgery is still the mainstay for comprehensive treatment for NSCLC and EC, but the prognosis is still poor as the results of cancer recurrence and distant metastasis. Neoadjuvant therapy refers to a single or combined treatment before surgery, aiming to improve the therapeutic effects of the traditional therapies. Unfortunately, the clinical outcomes and effects of neoadjuvant therapy are still controversial due to its apparent advantages and disadvantages, and different patients may respond differentially to the same scheme of neoadjuvant therapy, which makes it urgent and necessary to develop personalized scheme of neoadjuvant therapy for different individuals. Therefore, this review summarizes the novel schemes and strategies of neoadjuvant therapy, which may help to significantly improve of life quality of patients suffering from chest-related malignancies.

Decadal soil total carbon loss in northern hinterland of Tibetan Plateau.

As the largest and highest plateau in the world, ecosystems on the Tibetan Plateau (TP) imply fundamental ecological significance to the globe. Among the variety, alpine grassland ecosystem on the TP forms a critical part of the global ecosystem and its soil carbon accounts over nine tenths of ecosystem carbon. Revealing soil carbon dynamics and the underlying driving forces is vital for clarifying ecosystem carbon sequestration capacity on the TP. By selecting northern TP, the core region of the TP, this study investigates spatiotemporal dynamics of soil total carbon and the driving forces based on two phases of soil sampling data from the 2010s and the 2020s. The research findings show that soil total carbon density (STCD) in total-surface (0-30 cm) in the 2010s (8.85 ± 3.08 kg C m-2) significantly decreased to the 2020s (7.15 ± 2.90 kg C m-2), with a decreasing rate (ΔSTCD) of -0.17 ± 0.39 kg C m-2 yr-1. Moreover, in both periods, STCD exhibited a gradual increase with soil depth deepening, while ΔSTCD loss was more apparent in top-surface and mid-surface than in sub-surface. Spatially, ΔSTCD loss in alpine desert grassland was -0.41 ± 0.48 kg C m-2 yr-1, which is significantly higher than that in alpine grassland (-0.11 ± 0.31 kg C m-2 yr-1) or alpine meadow (-0.04 ± 0.28 kg C m-2 yr-1). The STCD in 2010s explained >30 % of variances in ΔSTCD among the set of covariates. Moreover, rising temperature aggravates ΔSTCD loss in alpine desert grassland, while enhanced precipitation alleviates ΔSTCD loss in alpine meadow. This study sheds light on the influences of climate and background carbon on soil total carbon loss, which can be benchmark for predicting carbon dynamics under future climate change scenarios.

Ti-Doped AgNbO3 as Novel Dense Diffusion Barriers of Limiting Current Oxygen Sensors.

The oxygen sensors with limiting current derived from a dense diffusion barrier have an excellent advantage of detecting oxygen partial pressure by controlling the ratio of air and fuel in combustion environments. Therefore, AgNb1-xTixO3-δ (wherein x varies from 0.1 to 0.3) was prepared as such a dense diffusion barrier layer for sensor application. Among the investigated compositions as a new condensed barrier for the diffusion of sensors, AgNb1-xTixO3-δ (x = 0.1, 0.2, 0.3) exhibits oxygen ionic conductivities from 1.37 × 10-4 to 5.78 × 10-3 S·cm-1 in the temperature range of 600-900 °C and outstanding stable electrochemical properties. Herein, we employ these novel materials as dense diffusion barriers and 8 mol % zirconia stabilized by yttria (8YSZ) as a solid-state electrolyte for the fabrication of the oxygen sensors with limiting current. We observed a direct connection between the limiting current and oxygen content within the interval of 0.5-5.0 mol % at 800 °C and a low working voltage. The increase of Ti-doping amount in AgNbO3 accelerates the sensing response to oxygen gas and promotes the service life of the sensor.

Herbivore exclusion stabilizes alpine grassland biomass production across spatial scales.

There is growing evidence that land-use management practices such as livestock grazing can strongly impact the local diversity, functioning, and stability of grassland communities. However, whether these impacts depend on environmental condition and propagate to larger spatial scales remains unclear. Using an 8-year grassland exclosure experiment conducted at nine sites in the Tibetan Plateau covering a large precipitation gradient, we found that herbivore exclusion increased the temporal stability of alpine grassland biomass production at both the local and larger (site) spatial scales. Higher local community stability was attributed to greater stability of dominant species, whereas higher stability at the larger scale was linked to higher spatial asynchrony of productivity among local communities. Additionally, sites with higher mean annual precipitation had lower dominant species stability and lower grassland stability at both the spatial scales considered. Our study provides novel evidence that livestock grazing can impair grassland stability across spatial scales and climatic gradients.

Resource co-limitation of community biomass but not structure of an alpine grassland.

Anthropogenic environmental changes are influencing the structure and function of many ecological communities, but their underlying mechanisms are often poorly understood. We conducted a 7-year field experiment to explore the ecological consequences of nitrogen (N) and phosphorous (P) enrichment in a high-altitude Tibetan alpine grassland. We found that the enrichment of both N and P, but not either alone, increased plant above- and belowground biomass. In contrast, N, but not P, enrichment reduced species richness and altered plant phylogenetic diversity and structure. Whereas plant species loss and changes in phylogenetic structure were mainly driven by higher soil manganese levels under N addition, they were mainly driven by increased plant belowground biomass under the addition of both N and P. Our study highlights the resource co-limitation of community biomass but not the structure of the study grassland, while also identifying soil metal toxicity and belowground competition as important mechanisms driving community changes following nutrient amendment.

Nitrogen enrichment differentially regulates the response of ecosystem stability to extreme dry versus wet events.

Extreme climate events, such as severe droughts and heavy rainfall, have profound impacts on the sustainable provision of ecosystem functions and services. However, how N enrichment interacts with discrete extreme climate events to affect ecosystem functions is largely unknown. Here, we investigated the responses of the temporal stability (i.e., resistance, recovery, and resilience) of aboveground net primary productivity (ANPP) in an alpine meadow to extreme dry and wet events under six N addition treatments (0, 2, 4, 8, 16, 32 g N m-2 year-1). We found that N addition had contrasting effects on the responses of ANPP to the extreme dry versus wet events, which resulted in no overall significant effects on ANPP stability across 2015-2019. Specifically, high N addition rates reduced the stability, resistance, and resilience of ANPP in response to extreme drought, whereas medium N addition rates increased ANPP stability and recovery in response to the extreme wet event. The main mechanisms underlying the response of ANPP to extreme drought and wet events were discrepant. Species richness, asynchrony, and dominant species resistance contributed most to the reduction of ANPP resistance to extreme drought, while species asynchrony and dominant and common species resilience contributed most to the decrease of ANPP resilience from extreme drought with N enrichment. The ANPP recovery from the extreme wet event was mainly explained by dominant and common species recovery. Our results provide strong evidence that N deposition mediates ecosystem stability in response to extreme dry and wet events in different ways and modulates the provisioning of grassland ecosystem functions under increasing extreme climate events.

Depth-dependent drivers of soil aggregate carbon across Tibetan alpine grasslands.

Elucidating the effects underlying soil organic carbon (SOC) variation is imperative for ascertaining the potential drivers of mitigating climate change. However, the drivers of variations in various SOC fractions (e.g., macroaggregate C, microaggregate C, and silt and clay C) at different soil depths remain poorly understood. Here, we investigated the effects and relative contributions of climatic, plant, edaphic, and microbial factors on soil aggregate C between the topsoil (0-10 cm) and subsoil (20-30 cm) across alpine grasslands on the Tibetan Plateau. Results showed that the C content of macroaggregates, microaggregates, and silt and clay fractions in the topsoil was 128.6 %, 49.6 %, and 242.4 % higher than that in the subsoil, respectively. Overall, plant properties were the most determinants controlling soil macroaggregate, microaggregate, and silt + clay associated C for both two soil depths, accounting for 32.2 %, 37.4 %, and 38.8 % of the variation, respectively, followed by edaphic, microbial, and climatic factors. The aggregate C of both soil depths was significantly related with the climatic, plant, edaphic, and microbial factors, but the relative importance of these determinants was soil-depth dependent. Specifically, the effects of plant root biomass and microbial (e.g., microbial biomass carbon and fungal diversity index) factors on each aggregate C weakened with soil depth, but the importance of edaphic factors (e.g., clay content, pH, and bulk density) strengthened with soil depth, except for the weakened effect of bulk density on the microaggregate C. And the effects of climatic factor (e.g., mean annual precipitation) on macroaggregate and microaggregate C increased with soil depth. Our results highlight differential drivers and their impacts on soil aggregate C between the topsoil and subsoil, which benefits biogeochemical models for more accurately forecasting soil C dynamics and its feedbacks to environmental changes.

Knockdown of TRIM44 inhibits the progression of ovarian cancer and is related to the FOXM1-EZH2 signaling pathway.

Background: Tripartite motif-containing protein 44 (TRIM44) was recently identified as a novel oncogene that is overexpressed in several types of human cancers. However, the biological functions of TRIM44 in epithelial ovarian cancer (EOC) remain unclear. Here, we aimed to investigate the role of TRIM44 in EOC and its clinical implications. Methods: TRIM44 was knocked down using shRNA transfection. In vitro proliferation, invasion, migration and apoptosis of ovarian cancer (OC) cells were detected by CCK8, colony formation assay, Transwell inserts and flow cytometry analysis. The growth ability of xenograft tumors was examined in vivo in a nude mouse metastatic tumor model. Finally, we performed gene chip analysis and ingenuity pathway analysis (IPA) to analyze the potential gene network. Results: High expression of TRIM44 was observed in EOC tissues. Knockdown of TRIM44 expression substantially suppressed the proliferation, migration, invasion and colony-forming ability of EOC cells in vitro and attenuated tumor growth in vivo. Mechanistic studies revealed that silencing TRIM44 dramatically downregulated the expression of FOXM1, EZH2, CCNE2, CCND3 and BIRC5 in EOC cells, at least in part through inactivation of the FOXM1-EZH2 signaling pathway. Conclusions: Collectively, these data suggest that downregulation of TRIM44 inhibits the progression of EOC through suppression of the FOXM1-EZH2 signaling pathway. These results provide novel insight into the role of TRIM44 in tumorigenesis and suggest that it could be a potential therapeutic target for ovarian carcinoma.

TMEM139 prevents NSCLC metastasis by inhibiting lysosomal degradation of E-cadherin.

Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases and has the highest mortality rate among all solid tumors. It is characterized by early metastasis, and investigations of the molecular mechanisms underlying the progression and metastasis of NSCLC are urgently needed for the development of therapeutic targets. Here, we report that the transmembrane protein TMEM139 is significantly downregulated in NSCLC and that reduced expression of TMEM139 is correlated with a poor prognosis in NSCLC patients. Mechanistically, we found that TMEM139 directly interacts with E-cadherin at the plasma membrane and at focal adhesion sites. Moreover, TMEM139 can prevent the lysosomal degradation of E-cadherin, which inhibits epithelial-mesenchymal transition, migration and invasion of NSCLC cells both in vitro and in vivo. Our study not only expands our understanding of NSCLC metastasis but also provides a foundation to develop novel therapeutic strategies.

Increased annual methane uptake driven by warmer winters in an alpine meadow.

Pronounced nongrowing season warming and changes in soil freeze-thaw (F-T) cycles can dramatically alter net methane (CH4 ) exchange rates between soils and the atmosphere. However, the magnitudes and drivers of warming impacts on CH4 uptake in different stages of the F-T cycle are poorly understood in cold alpine ecosystems, which have been found to be a net sink of atmospheric CH4 . Here, we reported a year-round ecosystem daily CH4 uptake in an alpine meadow on the Qinghai-Tibetan Plateau after a 5-year warming experiment that included a control, a low-level warming treatment (+2.4℃ at 5 cm soil depth), and a high-level warming treatment (+4.5℃ at 5 cm soil depth). We found that warming shortened the F-T cycle under the low-level warming and soils did not freeze under the high-level warming. Although both warming treatments increased the mean CH4 uptake rate, only the high-level warming significantly increased annual CH4 uptake compared to the control. The warming-induced stimulation of CH4 uptake mainly occurred in the cold season, which was mostly during spring thaw under low-level warming and during the frozen winter under high-level warming due to a longer period with thawed soil. We also found that warming significantly stimulated daily CH4 uptake mainly by reducing near-surface soil water content in the warm season, whereas both soil water content and temperature controlled daily CH4 uptake in different ways during the autumn freeze, frozen winter, and spring thaw periods of the control. Our study revealed a strong warming effect on CH4 uptake during the entire F-T cycle in the alpine meadow, especially the unfrozen winter. Our results also suggested the important roles of soil pH, available phosphorus, and methanotroph abundance in regulating annual CH4 uptake in response to warming, which should be incorporated into biogeochemical models for accurately forecasting CH4  fluxes under future climate scenarios.

CircKEAP1 Suppresses the Progression of Lung Adenocarcinoma via the miR-141-3p/KEAP1/NRF2 Axis.

BACKGROUND: Lung cancer is the leading cause of death from cancer, and lung adenocarcinoma (LUAD) is the most common form. Despite the great advances that has been made in the diagnosis and treatment for LUAD, the pathogenesis of LUAD remains unclear. In this study, we aimed to identify the function of circKEAP1 derived from the exon of KEAP1 in LUAD. METHODS: The expression profiles of circRNAs in LUAD tissues and adjacent non-tumor tissues were analyzed by Agilent Arraystar Human CircRNA microarray. The levels and prognostic values of circKEAP1 in tissues and cancer cell lines were determined by quantitative real-time PCR (qRT-PCR). Subsequently, the effects of circKEAP1 on tumor growth were investigated by functional experiments in vitro and in vivo. Mechanistically, the dual luciferase reporter assay, RNA pull-down, and RNA immunoprecipitation experiments were performed to confirm the interaction between circKEAP1 and miR-141-3p in LUAD. RESULTS: We found circKEAP1 was significantly downregulated in LUAD tissues and repressed tumor growth both in vitro and in vivo. Mechanistically, circKEAP1 competitively binds to miR-141-3p and relive miR-141-3p repression for its host gene, which activated the KEAP1/NRF2 signal pathway, and finally suppresses the tumor progress. Our findings suggest that circKEAP1 inhibits LUAD progression through circKEAP1/miR-141-3p/KEAP1 axis and it may serve as a novel method for the treatment of LUAD.

Symmetric Deformable Registration via Learning a Pseudomean for MR Brain Images.

Image registration is a fundamental task in medical imaging analysis, which is commonly used during image-guided interventions and data fusion. In this paper, we present a deep learning architecture to symmetrically learn and predict the deformation field between a pair of images in an unsupervised fashion. To achieve this, we design a deep regression network to predict a deformation field that can be used to align the template-subject image pair. Specifically, instead of estimating the single deformation pathway to align the images, herein, we predict two halfway deformations, which can move the original template and subject into a pseudomean space simultaneously. Therefore, we train a symmetric registration network (S-Net) in this paper. By using a symmetric strategy, the registration can be more accurate and robust particularly on the images with large anatomical variations. Moreover, the smoothness of the deformation is also significantly improved. Experimental results have demonstrated that the trained model can directly predict the symmetric deformations on new image pairs from different databases, consistently producing accurate and robust registration results.

Fatty acid oxidation is required for embryonic stem cell survival during metabolic stress.

Metabolic regulation is critical for the maintenance of pluripotency and the survival of embryonic stem cells (ESCs). The transcription factor Tfcp2l1 has emerged as a key factor for the naïve pluripotency of ESCs. Here, we report an unexpected role of Tfcp2l1 in metabolic regulation in ESCs-promoting the survival of ESCs through regulating fatty acid oxidation (FAO) under metabolic stress. Tfcp2l1 directly activates many metabolic genes in ESCs. Deletion of Tfcp2l1 leads to an FAO defect associated with upregulation of glucose uptake, the TCA cycle, and glutamine catabolism. Mechanistically, Tfcp2l1 activates FAO by inducing Cpt1a, a rate-limiting enzyme transporting free fatty acids into the mitochondria. ESCs with defective FAO are sensitive to cell death induced by glycolysis inhibition and glutamine deprivation. Moreover, the Tfcp2l1-Cpt1a-FAO axis promotes the survival of quiescent ESCs and diapause-like blastocysts induced by mTOR inhibition. Thus, our results reveal how ESCs orchestrate pluripotent and metabolic programs to ensure their survival in response to metabolic stress.

NF-κB-induced R-loop accumulation and DNA damage select for nucleotide excision repair deficiencies in adult T cell leukemia.

Constitutive NF-κB activation (NF-κBCA) confers survival and proliferation advantages to cancer cells and frequently occurs in T/B cell malignancies including adult T cell leukemia (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1). Counterintuitively, NF-κBCA by the HTLV-1 transactivator/oncoprotein Tax induces a senescence response, and HTLV-1 infections in culture mostly result in senescence or cell-cycle arrest due to NF-κBCA How NF-κBCA induces senescence, and how ATL cells maintain NF-κBCA and avert senescence, remain unclear. Here we report that NF-κBCA by Tax increases R-loop accumulation and DNA double-strand breaks, leading to senescence. R-loop reduction via RNase H1 overexpression, and short hairpin RNA silencing of two transcription-coupled nucleotide excision repair (TC-NER) endonucleases that are critical for R-loop excision-Xeroderma pigmentosum F (XPF) and XPG-attenuate Tax senescence, enabling HTLV-1-infected cells to proliferate. Our data indicate that ATL cells are often deficient in XPF, XPG, or both and are hypersensitive to ultraviolet irradiation. This TC-NER deficiency is found in all ATL types. Finally, ATL cells accumulate R-loops in abundance. Thus, TC-NER deficits are positively selected during HTLV-1 infection because they facilitate the outgrowth of infected cells initially and aid the proliferation of ATL cells with NF-κBCA later. We suggest that TC-NER deficits and excess R-loop accumulation represent specific vulnerabilities that may be targeted for ATL treatment.

Clinical efficacy and safety of apatinib as maintenance treatment in patients with advanced esophageal squamous cell carcinoma.

Background: To investigate the clinical efficacy, safety and prognostic factors of apatinib therapy as maintenance treatment in patients with advanced esophageal squamous cell carcinoma. Methods: We selected 46 patients with advanced esophageal squamous cell carcinoma treated with radiotherapy and chemotherapy in our hospital from January 2017 to February 2019, all of whom were treated with apatinib. We analyzed the clinical efficacy, adverse reactions and prognostic factors. Meanwhile, the expression of VEGFR-2 and NF-kB was detected by the immunohistochemical SABC method. Results: The oral treatment of apatinib in the VEGFR-2 and NF-kB positive groups was better than that in the negative groups. The disease control rate was 67.39%. The main adverse reactions were hypertension (60.87%). The degree of adverse reactions was mainly grade 1-2. Cox multivariate regression analysis showed that the degree of adverse reactions and ECOG score were independent factors affecting OS in patients with advanced esophageal squamous cell carcinoma. Conclusion: The positive expression of VEGFR-2 and NF-kB is expected to be the molecular target of oral apatinib targeted therapy for esophageal cancer. Apatinib has a certain clinical effect as the maintenance treatment for advanced esophageal squamous cell carcinoma patients, with mild adverse reactions and high safety.

Segmenting Diabetic Retinopathy Lesions in Multispectral Images Using Low-Dimensional Spatial-Spectral Matrix Representation.

Multispectral imaging (MSI) provides a sequence of en-face fundus spectral slices and allows for the examination of structures and signatures throughout the thickness of retina to characterize diabetic retinopathy (DR) lesions comprehensively. Manual interpretation of MSI images is commonly conducted by qualitatively analyzing both the spatial and spectral properties of multiple spectral slices. Meanwhile, there exist few computer-based algorithms that can effectively exploit the spatial and spectral information of MSI images for the diagnosis of DR. We propose a new approach that can quantify the spatial-spectral features of MSI retinal images for automatic DR lesion segmentation. It combines a generalized low-rank approximation of matrices with a supervised regularization term to generate low-dimensional spatial-spectral representations using the feature vectors in all spectral slices. Experimental results showed that the proposed approach is very effective for the segmentation of DR lesions in MSI images, which suggests it as an interesting tool for assisting ophthalmologists in diagnosing, analyzing, and managing DR lesions in MSI.

Application effect of apatinib in patients with failure of standard treatment for advanced malignant tumours.

BACKGROUND: In recent years, targeted therapy has received widespread attention. Among these therapies, anti-angiogenic targeted drugs have become one of the hotspots of research. Apatinib is a novel oral small molecule anti-angiogenic agent that has been clinically tested in a variety of solid tumours. The aim of this study was to investigate the efficacy of apatinib in patients with advanced malignant tumours and failure of standard therapy. METHODS: We collected 41 patients with advanced malignant tumours in our department; all tumours were pathologically confirmed as malignant. All patients received apatinib after failure of standard therapy: 500 mg/dose, one dose/d, orally 30 min after a meal, until progressive disease or intolerable adverse reactions occurred. When there was a second- or third-degree adverse reaction associated with apatinib during treatment, apatinib treatment could be suspended or reduced to 250 mg/dose. Clinical efficacy and progression-free survival were assessed according to RECIST1.1, and adverse reactions were observed. RESULTS: Efficacy assessment was available for 31 patients with a median progression-free survival time of 2.66 months; the objective response rate and disease control rates were 16.1 and 64.5%, respectively. The disease control rates of the patients with lower Eastern Cooperative Oncology Group scores (1-2 points) and with fewer metastatic sites (< 3 sites) were higher than those of the patients with higher scores (3 points) and with more metastatic sites (≥3 sites), respectively (all P < 0.05). The most common adverse reactions were hypertension, neutropenia and hand-foot syndrome. CONCLUSION: For patients with advanced malignant tumours with failure of standard therapy, administration of apatinib can still result in good efficacy. The efficacy of apatinib is better in patients with a higher performance status and lower degree of tumour progression.

Mitochondrial dynamics and mitophagy are necessary for proper invasive growth in rice blast.

Magnaporthe oryzae causes blast disease, which is one of the most devastating infections in rice and several important cereal crops. Magnaporthe oryzae needs to coordinate gene regulation, morphological changes, nutrient acquisition and host evasion in order to invade and proliferate within the plant tissues. Thus far, the molecular mechanisms underlying the regulation of invasive growth in planta have remained largely unknown. We identified a precise filamentous-punctate-filamentous cycle in mitochondrial morphology during Magnaporthe-rice interaction. Interestingly, disruption of such mitochondrial dynamics by deletion of genes regulating either the mitochondrial fusion (MoFzo1) or fission (MoDnm1) machinery, or inhibition of mitochondrial fission using Mdivi-1 caused significant reduction in M. oryzae pathogenicity. Furthermore, exogenous carbon source(s) but not antioxidant treatment delayed such mitochondrial dynamics/transition during invasive growth. In contrast, carbon starvation induced the breakdown of the mitochondrial network and led to more punctate mitochondria in vitro. Such nutrient-based regulation of organellar dynamics preceded MoAtg24-mediated mitophagy, which was found to be essential for proper biotrophic development and invasive growth in planta. We propose that precise mitochondrial dynamics and mitophagy occur during the transition from biotrophy to necrotrophy and are required for proper induction and establishment of the blast disease in rice.

CircVRK1 regulates tumor progression and radioresistance in esophageal squamous cell carcinoma by regulating miR-624-3p/PTEN/PI3K/AKT signaling pathway.

As a novel class of noncoding RNAs (ncRNAs), circular RNAs (circRNAs) have been verified to be potential biomarkers and therapeutic targets for human malignant tumors. However, the thorough understanding of circRNAs in the progression of esophageal squamous cell carcinoma (ESCC) still needs to be improved. This study focused on exploring the function and mechanism of circVRK1 in ESCC. At first, we examined the expression level of circVRK1 in ESCC tissues and cell lines with qRT-PCR. We found that circVRK1 was downregulated in ESCC tissues and cell lines. Kaplan-Meier method was used to analyze the correlation between circVRK1 expression and the overall survival of ESCC patients. Functionally, overexpression of circVRK1 suppressed the cell proliferation, migration and epithelial-mesenchymal transition (EMT) and reversed the radioresistance. Therefore, we identified the tumor suppressive role of circVRK1 in ESCC progression. Mechanistically, circVRK1 positively regulated PTEN by acting as a molecular sponge of miR-624-3p. Moreover, circVRK1 decreased the activity of PI3K/AKT signaling pathway by upregulating PTEN. Rescue assays were carried out to confirm the function of circVRK1-miR-624-3p-PTEN axis in ESCC progression. Our findings showed that circVRK1 suppressed ESCC progression by regulating miR-624-3p/PTEN axis and PI3K/AKT signaling pathway, suggesting the potential therapeutic value of circVRK1 for ESCC.

Effect of H2 SO4 Solution Treatment on Adhesion, Charge Transfer, and Catalytic Performance of Screen-Printed PEDOT:PSS.

Post-treatment was performed for poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) films screen-printed on fluorine-doped tin oxide (FTO) substrates, to improve their charge transfer efficiency. Different H2 SO4 solutions, including concentrated H2 SO4 and H2 SO4 diluted with H2 O or dimethyl sulfoxide (DMSO), were adopted during the post-treatment. The adhesion of the as-treated films was evaluated by adhesive tape peeling tests, the surface morphology and vertical charge transfer from the films to the substrates were investigated by current-sensing atomic force microscopy, and the catalytic activities toward I3- reduction of PEDOT:PSS films were characterized by electrochemical measurements. It is discovered that selecting proper H2 SO4 solutions is crucial to improve the charge transfer efficiency and catalytic performance while maintaining reliable adhesion of the film on the substrates, with H2 SO4 /DMSO performing best as the solution for post-treatment. A mechanistic explanationis proposed based on different interactions among solution, PEDOT:PSS, and the substrate for various post-treatment solutions.