An open-label, prospective trial to evaluate the efficacy and safety of ixazomib in combination with cyclophosphamide and dexamethasone in patients with newly diagnosed POEMS syndrome.

This open-label, prospective trial evaluated the combination of ixazomib, cyclophosphamide and dexamethasone (ICD) in 12 newly diagnosed POEMS syndrome patients. The study is registered with the Chinese Clinical Trials Registry (ChiCTR2000030072). The treatment protocol consisted of 12 cycles of the ICD regimen compromising ixazomib (4 mg on Days 1, 8 and 15), oral cyclophosphamide (300 mg on Days 1, 8 and 15) and dexamethasone (20 mg weekly). A total of 12 patients received a median of 10 (range: 3-23) cycles of the ICD regimen. The haematological response could be evaluated in 10 patients. The overall haematological response rate was 80% (8/10), with 30% (3/10) achieving complete haematological response, and the overall serum VEGF response rate and neurological response were 100% and 83.3% respectively. Two patients experienced grade 3/4 AEs, including diarrhoea (n = 1) and leukopenia (n = 1). The combination of ixazomib, cyclophosphamide and dexamethasone demonstrated both efficacy and safety in newly diagnosed POEMS syndrome, making it a viable treatment option.

Ethylene controls three-dimensional growth involving reduced auxin levels in the moss Physcomitrium patens.

The conquest of land by plants was concomitant with, and possibly enabled by, the evolution of three-dimensional (3D) growth. The moss Physcomitrium patens provides a model system for elucidating molecular mechanisms in the initiation of 3D growth. Here, we investigate whether the phytohormone ethylene, which is believed to have been a signal before land plant emergence, plays a role in 3D growth regulation in P. patens. We report ethylene controls 3D gametophore formation, based on results from exogenously applied ethylene and genetic manipulation of PpEIN2, which is a central component in the ethylene signaling pathway. Overexpression (OE) of PpEIN2 activates ethylene responses and leads to earlier formation of gametophores with fewer gametophores produced thereafter, phenocopying ethylene-treated wild-type. Conversely, Ppein2 knockout mutants, which are ethylene insensitive, show initially delayed gametophore formation with more gametophores produced later. Furthermore, pharmacological and biochemical analyses reveal auxin levels are decreased in the OE lines but increased in the knockout mutants. Our results suggest that evolutionarily, ethylene and auxin molecular networks were recruited to build the plant body plan in ancestral land plants. This might have played a role in enabling ancient plants to acclimate to the continental surfaces of the planet.

Photocatalytic Proton-Coupled Electron Transfer Enabled Radical Cyclization for Isoquinoline-1,3-diones Synthesis.

Radical cyclization has been demonstrated to be an efficient method to access functionalized heterocycles from easily accessible raw materials. Described herein is the development of a photocatalytic proton-coupled electron transfer (PCET) strategy for the synthesis of isoquinoline-1,3-diones using readily prepared naphthalimide (NI)-based organic photocatalysts. The process features free metal-complex photocatalysts, acids, and mild reaction conditions. This mild radical cyclization protocol has a broad substrate scope and can be effectively applied to a variety of medicinally relevant substrates. Furthermore, control experiments were conducted to elucidate the mechanism of this visible light-induced methodology.

Developing a Prognostic Model for Primary Biliary Cholangitis Based on a Random Survival Forest Model.

Background: Primary biliary cholangitis (PBC) is a rare autoimmune liver disease with few effective treatments and a poor prognosis, and its incidence is on the rise. There is an urgent need for more targeted treatment strategies to accurately identify high-risk patients. The use of stochastic survival forest models in machine learning is an innovative approach to constructing a prognostic model for PBC that can improve the prognosis by identifying high-risk patients for targeted treatment. Method: Based on the inclusion and exclusion criteria, the clinical data and follow-up data of patients diagnosed with PBC-associated cirrhosis between January 2011 and December 2021 at Taizhou Hospital of Zhejiang Province were retrospectively collected and analyzed. Data analyses and random survival forest model construction were based on the R language. Result: Through a Cox univariate regression analysis of 90 included samples and 46 variables, 17 variables with p-values <0.1 were selected for initial model construction. The out-of-bag (OOB) performance error was 0.2094, and K-fold cross-validation yielded an internal validation C-index of 0.8182. Through model selection, cholinesterase, bile acid, the white blood cell count, total bilirubin, and albumin were chosen for the final predictive model, with a final OOB performance error of 0.2002 and C-index of 0.7805. Using the final model, patients were stratified into high- and low-risk groups, which showed significant differences with a P value <0.0001. The area under the curve was used to evaluate the predictive ability for patients in the first, third, and fifth years, with respective results of 0.9595, 0.8898, and 0.9088. Conclusion: The present study constructed a prognostic model for PBC-associated cirrhosis patients using a random survival forest model, which accurately stratified patients into low- and high-risk groups. Treatment strategies can thus be more targeted, leading to improved outcomes for high-risk patients.

The inhibitory effects of ginsenoside Rd on the human glioma U251 cells and its underlying mechanisms.

OBJECTIVE: The current study was designed to investigate the inhibitory effects of ginsenoside Rd (Gs-Rd) on human glioma U251 cells in vitro and its possible underlying mechanisms. METHODS: The groups included blank control group, low concentration Gs-Rd treatment group (20 µM), mid concentration Gs-Rd treatment group (40 µM), and high concentration Gs-Rd treatment group (80 µM). The proliferative activity of human glioma U251 cells was detected by the MTT assay. Flow cytometry was performed to measure cell apoptosis of human glioma U251 cells. In addition, the ELISA assay was used to measure the telomerase activities in different groups on 24 hours, 48 hours, and 72 hours. Furthermore, real-time quantitative polymerase chain reaction (RT-PCR) and Western blot analysis were performed to measure the expression of Bcl-2, human telomerase catalytic subunit (hTERT), and caspase-3 in different groups on 48 hours at both messenger RNA (mRNA) and protein levels. RESULTS: The proliferation of U251 cells was inhibited by Gs-Rd with different concentrations in the dose- and time-dependent manners. In addition, Gs-Rd promoted U251 cell apoptosis rate in a dose-dependent manner. Gs-Rd with different concentrations (20 µM, 40 µM, and 80 µM) significantly enhanced the expression of teleomerase on 24 hours and 48 hours. In addition, Gs-Rd with different concentrations significantly increased caspase-3 and decreased Bcl-2 and hTERT expressions at both mRNA and protein levels. CONCLUSION: The Gs-Rd can remarkably inhibit the proliferation and promote cell apoptosis of human glioma U251 cells. The possible underlying mechanisms could be related to inhibiting telomerase activity, downregulating expression of Bcl-2 and hTERT, and upregulating expression of caspase-3 of human glioma U251 cells.

microRNA-383 regulates cell viability and apoptosis by mediating Wnt/ß-catenin signaling pathway in non-small cell lung cancer.

The aim of this study was to investigate the roles of microRNA-383 (miRNA-383) in progression of non-small cell lung cancer (NSCLC) and the potential mechanism. The expressions of miR-383 and Wnt1 protein were detected in lung cancer tissues and cells by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. After the transfection of miR-383 mimics, si-Wnt1 or miR-383+Wnt1, the viability and apoptosis of NSCLC cells were detected by cell counting kit-8 and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, respectively. The interaction between miR-383 and Wnt1 was investigated by luciferase activity and Western blot analysis. Cells stably transfected with miR-383 mimics were inoculated into the right axillary of nude mice by subcutaneous injection. The tumor volume and weight were measured, and the expressions of miR-383, Wnt1, ß-catenin, and cyclin D1 were detected by qRT-PCR and Western blot analysis. The expression of miR-383 was significantly decreased, and the level of Wnt1 was significantly increased (P < 0.05) in lung cancer tissues and cells. Upregulation of miR-383 or inhibition of Wnt1 expression inhibited the cell viability and induce apoptosis in NSCLC cells. Moreover, Wnt1 was the target gene of miR-383, and its overexpression weakened the regulatory effect of miR-383 on cell viability and apoptosis in NSCLC cells. Besides, the addition of miR-383 decreased the tumor volume and size and inhibited the expressions of Wnt1, ß-catenin, and cyclin D1 at the protein level in nude mice. Collectively, miR-383 induced apoptosis and inhibited cell viability as well as tumorigenic capacity in nude mice via regulating the Wnt/ß-catenin signaling pathway.

Circular RNA circ-PRKCI functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-3680-3p in esophageal squamous cell carcinoma.

Circular RNA (circRNA) is a new noncoding RNAs and plays an important role in many pathological processes. Recently, studies have shown that circular RNA_PRKCI (circ-PRKCI) regulates cell proliferation and cell migration of tumor cells. Esophageal carcinoma is a highly malignant digestive tract tumor, which is divided into esophageal adenocarcinoma and esophageal squamous cell carcinoma. In this study, we studied whether circ-PRKCI might influence cell proliferation and cell migration in esophageal squamous cell carcinoma. Quantitative reverse transcription PCR was performed to detect the relative expression of circ-PRKCI in five cases of esophageal squamous cell carcinoma and five cases of paired adjacent normal tissues. RNA immunoprecipitation assay and Luciferase assay confirm the direct interaction between miR-3680-3p and AKT3 or circ-PRKCI. Ethynyldeoxyuridine assays and cell counting Kit-8 were performed to evaluate the effect of miR-3680-3p or circ-PRKCI on cell proliferation, transwell assays were also performed to detect migration in vitro. We found circ-PRKCI is obviously upregulated in esophageal squamous cell carcinoma and upregulation of circ-PRKCI stimulated cell migration and proliferation of ESCC cells. In the mechanism, we confirm that circ-PRKCI, as a molecular sponge of miR-3680-3p, upregulates the expression of AKT. In conclusion, our current studies have been revealing that circ-PRKCI/miR-3680-3p/AKT3 regulatory network plays an important role in esophageal squamous cell carcinoma and that provide new insights into the pathogenesis of esophageal squamous cell carcinoma.

Lipoxin A4 Methyl Ester Reduces Early Brain Injury by Inhibition of the Nuclear Factor Kappa B (NF-κB)-Dependent Matrix Metallopeptidase 9 (MMP-9) Pathway in a Rat Model of Intracerebral Hemorrhage.

BACKGROUND Intracerebral hemorrhage (ICH) is associated with inflammation and disruption of the blood-brain barrier (BBB). Lipoxin A4 methyl ester (LXA4 ME), is a stable synthetic analog of lipoxin with anti-inflammatory properties. This study aimed to investigate the effects of LXA4 ME in a rat model of ICH. MATERIAL AND METHODS Male Sprague-Dawley rats (n=120), between 12-13 weeks of age, were divided into the sham group (sham-operated), the vehicle-treated group (ICH+vehicle), the LXA4 ME-L group (ICH+low-dose LXA4 ME, 10 ng/d), and the LXA4 ME-H group (ICH+high-dose LXA4 ME, 100 ng/d). The ICH model was created by injection of autologous blood into the right basal ganglia. LXA4 ME was injected into the ventricle 10 min after the development of ICH. A modified neurological severity score (mNSS), rotarod latencies, and brain water content were used to evaluate the rats. The TUNEL assay measured neuronal cell death. Western blot was used to measure protein expression of nuclear factor kappa B (NF-kappaB), matrix metalloproteinase-9 (MMP-9), zonula occludens-1 (ZO-1), and claudin-5. RESULTS In the rat model of ICH, treatment with LXA4 ME reduced the levels of proinflammatory cytokines, improved neurologic function, reduced neuronal apoptosis, and reduced cerebral edema associated with damage to the BBB, and reduced the expression levels of NF-kB, MMP-9, ZO-1, and claudin-5. CONCLUSIONS In a rat model of ICH, treatment with LXA4 reduced early brain injury and protected the BBB by inhibiting the NF-kappaB-dependent MMP-9 pathway.

Effect of GDF11 on proliferation and apoptosis of esophageal cancer cells.

This study was aimed at investigating the effect of growth differentiation factor 11 (GDF11) on the proliferation and apoptosis of esophageal cancer cells. Serum levels of GDF11 in esophageal cancer patients were determined with ELISA kits, and the correlation between serum GDF11 and pathological features of esophageal cancer were determined. The effect of recombinant GDF11 on the growth of esophageal cancer cells was measured by CCK6 method. In order to investigate the effect of recombinant GDF11 on the proliferation and apoptosis of esophageal cancer cells, the expression of apoptosis-promoting protein Bax and proliferative-associated protein Bcl-2 in esophageal cancer cells were determined using western blot. Moreover, GDF11 was used to treat esophageal cancer cells, and its effect on proliferation and apoptosis was determined with MTT assay and flow cytometry, respectively. The serum content of GDF11 was much less in esophageal cancer patients than in the control group. Esophageal GDF II in cancer patients was correlated with cancer differentiation: the higher the degree of differentiation, the higher the content of GDF11. GDF11 inhibits proliferation and apoptosis of esophageal cancer cells.

Systemic immune-inflammation index predicting chemoradiation resistance and poor outcome in patients with stage III non-small cell lung cancer.

BACKGROUND: There is increasing evidence that the existence of systemic inflammation response is correlated with poor prognosis in several solid tumors. The aim of this retrospective study was to investigate the association between systemic immune-inflammation index (SII) and therapy response and overall survival in patients with stage III non-small cell lung cancer (NSCLC). The prognostic values of neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and prognostic nutritional index (PNI) were also evaluated. METHODS: In total, 332 patients with new diagnosis of stage III NSCLC were included in this retrospective analysis. SII was defined as platelet counts × neutrophil counts/lymphocyte counts. Receiver operating characteristic (ROC) curve was used to evaluate the optimal cut-off value for SII, NLR, PLR and PNI. Univariate and multivariate survival analysis were performed to identify the factors correlated with overall survival. RESULTS: Applying cut-offs of ≥ 660 (SII), ≥ 3.57 (NLR), ≥ 147 (PLR), ≤ 52.95 (PNI), SII ≥ 660 was significantly correlated with worse ECOG PS (< 0.001), higher T stage (< 0.001), advanced clinical stage (p = 0.019), and lower response rate (p = 0.018). In univariate analysis, SII ≥ 660, NLR ≥ 3.57, PLR ≥ 147, and PNI ≤ 52.95 were significantly associated with worse overall survival (p all < 0.001). Patients with SII ≥ 660 had a median overall survival of 10 months, and patients with SII < 660 showed a median overall survival of 30 months. In multivariate analysis only ECOG PS (HR, 1.744; 95% CI 1.158-2.626; p = 0.008), T stage (HR, 1.332; 95% CI 1.032-1.718; p = 0.028), N stage (HR, 1.848; 95% CI 1.113-3.068; p = 0.018), SII (HR, 2.105; 95% CI 1.481-2.741; p < 0.001) and NLR ≥ 3.57 (HR, 1.934; 95% CI 1.448-2.585; p < 0.001) were independently correlated with overall survival. CONCLUSIONS: This study demonstrates that the SII is an independent prognostic indicator of poor outcomes for patients with stage III NSCLC and is superior to other inflammation-based factors in terms of prognostic ability.

High expression of long non-coding RNA AFAP1-AS1 predicts chemoradioresistance and poor prognosis in patients with esophageal squamous cell carcinoma treated with definitive chemoradiotherapy.

To evaluate the clinical significance of lncRNAs in the resistance to cisplatin-based chemoradiotherapy in esophageal squamous cell carcinoma (ESCC). We focused on lncRNAs which were frequently reported in ESCC or were involved in chemoradiotherapy resistance. LncRNA expressions were examined in paired cisplatin-resistant and parental ESCC cell lines. Dysregulated lncRNAs were further measured in 162 pretreatment biopsy specimens of ESCC who received definitive chemoradiotherapy (dCRT). Then the correlations between lncRNA expression and response to dCRT and prognosis were analyzed. Three lncRNAs (AFAP1-AS1, UCA1, HOTAIR) were found to be deregulated in cisplatin-resistant cells compared with their parent cells. AFAP1-AS1 was significantly up-regulated in tumor tissues compared with adjacent normal tissues (P = 0.006). Furthermore, overexpression of AFAP1-AS1 was closely associated with lymph node metastasis (P < 0.001), distant metastasis (P = 0.016), advanced clinical stage (P = 0.002), and response to dCRT (P < 0.001). Kaplan-Meier survival analysis revealed that high expression of AFAP1-AS1 was significantly associated with shorter progression free survival (PFS) (median, 15 months vs. 27 months, P < 0.001) and overall survival (OS) (median, 29 months vs. 42 months, P < 0.001). In the multivariate analysis, high expression of AFAP1-AS1 was found to be an independent risk factor to predict poor PFS (HR, 1.626; P = 0.027) and OS (HR, 1.888; P = 0.004). Thus, high expression of AFAP1-AS1 could serve as a potential biomarker to predict tumor response and survival. Determination of this lncRNA expression might be useful for selection ESCC patients for dCRT. © 2016 The Authors. Molecular Carcinogenesis published by Wiley Periodicals, Inc.

Gambogic acid enhances the radiosensitivity of human esophageal cancer cells by inducing reactive oxygen species via targeting Akt/mTOR pathway.

Radiotherapy is a widespread treatment in human solid tumors. However, therapy resistance and poor prognosis are still problems. Gambogic acid (GA), extracted from the dried yellow resin of gamboges, has an anticancer effect against various types of cancer cells. To explore the radiosensitivity of GA on esophageal cancer cell line TE13, cell viability was tested by Cell Counting Kit-8 (CCK-8) assay, colony formation assay was used to assess the effects of GA on the radiosensitivity of TE13, and flow cytometry was performed to meter the percentage of apoptosis. The protein levels of microtubule-associated protein 1 light chain 3 (LC3), caspase3, caspase8, casepase9, pAkt, and p-mammalian target of rapamycin (p-mTOR) were tested using Western blot. The distribution of LC3 was detected by immunofluorescence. Additionally, we also examined reactive oxygen species (ROS) expression by laser scanning confocal microscope (LSCM). The cells were transfected with adenovial vector to monitor the autophagy through the expression of green fluorescent protein (GFP-red fluroscent protein (RFP)-LC3. The rates of apoptotic cells in combined-treated TE13 increased significantly compared with the control groups in accordance with the results of Western blot. The clonogenic survival assay showed that GA enhances radiosensitivity with a sensitizing enhancement ratio (SER) of 1.217 and 1.436 at different concentrations. The LC3-II protein level increased in the combined group indicating the increase of autophagy incidence, and the results of GFP-RFP-LC3 experiment showed that GA may block the process of autophagic flux in TE13 cells. Moreover, we successfully demonstrated that ROS is involved in the induction of autophagy. ROS-mediated autophagy depends on the inhibition of the Akt/mTOR pathway. Taken together, GA induced radiosensitivity involves autophagy and apoptosis which are regulated by ROS hypergeneration and Akt/mTOR inhibition.

Deep learning assists detection of esophageal cancer and precursor lesions in a prospective, randomized controlled study.

Endoscopy is the primary modality for detecting asymptomatic esophageal squamous cell carcinoma (ESCC) and precancerous lesions. Improving detection rate remains challenging. We developed a system based on deep convolutional neural networks (CNNs) for detecting esophageal cancer and precancerous lesions [high-risk esophageal lesions (HrELs)] and validated its efficacy in improving HrEL detection rate in clinical practice (trial registration ChiCTR2100044126 at www.chictr.org.cn). Between April 2021 and March 2022, 3117 patients ≥50 years old were consecutively recruited from Taizhou Hospital, Zhejiang Province, and randomly assigned 1:1 to an experimental group (CNN-assisted endoscopy) or a control group (unassisted endoscopy) based on block randomization. The primary endpoint was the HrEL detection rate. In the intention-to-treat population, the HrEL detection rate [28 of 1556 (1.8%)] was significantly higher in the experimental group than in the control group [14 of 1561 (0.9%), P = 0.029], and the experimental group detection rate was twice that of the control group. Similar findings were observed between the experimental and control groups [28 of 1524 (1.9%) versus 13 of 1534 (0.9%), respectively; P = 0.021]. The system's sensitivity, specificity, and accuracy for detecting HrELs were 89.7, 98.5, and 98.2%, respectively. No adverse events occurred. The proposed system thus improved HrEL detection rate during endoscopy and was safe. Deep learning assistance may enhance early diagnosis and treatment of esophageal cancer and may become a useful tool for esophageal cancer screening.

Development and internal validation of a nomogram for predicting survival of nonoperative EGFR-positive locally advanced elderly esophageal cancers.

Purpose: This study aims to develop and validate a prediction model for non-operative, epidermal growth factor receptor (EGFR)-positive, locally advanced elderly esophageal cancer (LAEEC). Methods: A total of 80 EGFR-positive LAEEC patients were included in the study. All patients underwent radiotherapy, while 41 cases received icotinib concurrent systemic therapy. A nomogram was established using univariable and multivariable Cox analyses. The model's efficacy was assessed through area under curve (AUC) values, receiver operating characteristic (ROC) curves at different time points, time-dependent AUC (tAUC), calibration curves, and clinical decision curves. Bootstrap resampling and out-of-bag (OOB) cross-validation methods were employed to verify the model's robustness. Subgroup survival analysis was also conducted. Results: Univariable and multivariable Cox analyses revealed that icotinib, stage, and ECOG score were independent prognostic factors for LAEEC patients. The AUCs of model-based prediction scoring (PS) for 1-, 2-, and 3-year overall survival (OS) were 0.852, 0.827, and 0.792, respectively. Calibration curves demonstrated that the predicted mortality was consistent with the actual mortality. The time-dependent AUC of the model exceeded 0.75, and the internal cross-validation calibration curves showed good agreement between predicted and actual mortality. Clinical decision curves indicated that the model had a substantial net clinical benefit within a threshold probability range of 0.2 to 0.8. Model-based risk stratification analysis demonstrated the model's excellent ability to distinguish survival risk. Further subgroup analyses showed that icotinib significantly improved survival in patients with stage III and ECOG score of 1 (HR 0.122, P<0.001). Conclusions: Our nomogram model effectively predicts the overall survival of LAEEC patients, and the benefits of icotinib were found in the clinical stage III population with good ECOG scores.

A novel ADA-coated UCNPs@NB sensing platform combined with nucleic acid amplification for rapid detection of Escherichia coli.

In this study, we reported a novel sensing platform based on fluorescence quenching composed of alendronic acid (ADA) coated upconversion nanoparticles (UCNPs) and Nile Blue (NB) combined with polymerase chain reaction (PCR) for rapid, sensitive, and specific detection of Escherichia coli (E. coli). As a fluorescence acceptor, NB has a broad absorption band and can quench upconversion fluorescence intensity at 544 nm and 658 nm based on IFE. PCR is a double-stranded DNA (dsDNA) amplification technique with high specificity. The NB-dsDNA complex can be formed by intercalation of NB between base pairs and groove of dsDNA, leading to upconversion fluorescence recovery. The ADA-coated UCNPs@NB sensing platform achieved to detect E. coli in 1.5 h, with a lower limit of detection (33 CFU mL-1). In addition, the sensitivity of the ADA@UCNPs-NB fluorescence sensor under different PCR cycle numbers was discussed. The results showed that the proposed sensor could effectively shorten the assay time (1.0 h) while maintaining excellent sensitivity. This study demonstrated a rapid and sensitive analytical method for detecting E. coli in chicken, providing a reference for constructing PCR fluorescence sensors.

Plasma Thioredoxin Reductase as a Potential Biomarker for Gynecologic Cancer.

BACKGROUND: According to previous literatures, plasma thioredoxin reductase (TrxR) level was significantly elevated in various malignant tumors and serve as a potential biomarker for diagnosis and prognostic prediction. However, there is little awareness of the clinical value of plasma TrxR in gynecologic malignancies. In the present study, we aim to evaluate the diagnostic accuracy of plasma TrxR in gynecologic cancer and explore its role in treatment surveillance. METHODS: We retrospectively enrolled 134 patients with gynecologic cancer and 79 patients with benign gynecologic disease. The difference of plasma TrxR activity and tumor markers level between two groups was compared using Mann-Whitney U test. By detecting pretreatment and post-treatment level of TrxR and conventional tumor markers, we further assessed the change trend of them with the Wilcoxon signed-ranks test. RESULTS: Compared with benign control [5.7 (5, 6.6) U/mL], statistically significant increase of TrxR activity was observed in gynecologic cancer group [8.4 (7.25, 9.825) U/mL] (P < .0001), regardless of age and stage. On the basis of receiver operating characteristic (ROC) curves, we found plasma TrxR shows the highest diagnostic efficacy for distinguishing malignancy with benign disease, with an area under the curve (AUC) of 0.823 (95% confidence interval [CI] = 0.767-0.878), in the whole cohort. Besides, patients receiving treatment previously [8 (6.5, 9) U/mL] had a decreased TrxR level relative to treatment-native patients [9.9 (8.6, 10.85) U/mL]. Furthermore, follow-up data showed that plasma TrxR level would be evidently decreased after two courses of antitumor therapy (P < .0001), which is consistent with the downward trend of conventional tumor markers. CONCLUSION: Collectively, all these results demonstrated plasma TrxR is an effective parameter for gynecologic cancer diagnosis and concurrently acts as a promising biomarker for treatment response assessment.

Development of a Dual Mode UCNPs-MB Biosensor in Combination with PCR for Sensitive Detection of Salmonella.

In recent years, the high prevalence of Salmonella has emerged as a serious threat to public safety, prompting attempts to utilize accurate, rapid, and direct methods to ensure food safety. In this study, a multifunctional platform featuring dual-mode detection channels (colorimetric-fluorescence) combined with polymer chain reaction (PCR) was proposed for the sensitive and rapid detection of Salmonella. Additionally, the colorimetric measurements were achieved by color changes induced by methylene blue (MB) insertion into the double-stranded DNA, and the fluorescence measurements were performed by internal filter effect (IFE)-induced fluorescence quenching of upconversion nanoparticles (UCNPs) by MB. The results showed that the IFE and PCR amplification processes improved the sensitivity of the sensor towards Salmonella detection, with a limit of detection (LOD) of 21.8 CFU/mL. Moreover, this colorimetric-fluorescence dual-mode PCR biosensor was applied to determine Salmonella in food samples, such as chicken, egg, and fish, which produced satisfactory results. Overall, the present study results demonstrate the potential for combining PCR amplification with IFE to develop an efficient and reliable dual-mode analysis platform to safeguard food security.

Role of ferroptosis in colorectal cancer.

Colorectal cancer (CRC) is the second deadliest cancer and the third-most common malignancy in the world. Surgery, chemotherapy, and targeted therapy have been widely used to treat CRC, but some patients still develop resistance to these treatments. Ferroptosis is a novel non-apoptotic form of cell death. It is an iron-dependent non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species and has been suggested to play a role in reversing resistance to anticancer drugs. This review summarizes recent advances in the prognostic role of ferroptosis in CRC and the mechanism of action in CRC.

Direct observation of highly effective hydrogen isotope separation at active metal sites by in situ DRIFT spectroscopy.

In situ diffuse reflectance infrared Fourier transform (DRIFT) spectroscopy was developed for the first time to observe the hydrogen isotope separation behavior at active CuI sites within CuI-MFU-4l, and clear evidence of the preferential adsorption of D2 over H2 was directly captured. More importantly, our results show direct spectral proof to clarify the chemical affinity quantum sieving mechanism of hydrogen isotope separation within porous adsorbents.

Nitrite stimulates HONO and NOx but not N2O emissions in Chinese agricultural soils during nitrification.

The long-lived greenhouse gas nitrous oxide (N2O) and short-lived reactive nitrogen (Nr) gases such as ammonia (NH3), nitrous acid (HONO), and nitrogen oxides (NOx) are produced and emitted from fertilized soils and play a critical role for climate warming and air quality. However, only few studies have quantified the production and emission potentials for long- and short-lived gaseous nitrogen (N) species simultaneously in agricultural soils. To link the gaseous N species to intermediate N compounds [ammonium (NH4+), hydroxylamine (NH2OH), and nitrite (NO2-)] and estimate their temperature change potential, ex-situ dry-out experiments were conducted with three Chinese agricultural soils. We found that HONO and NOx (NO + NO2) emissions mainly depend on NO2-, while NH3 and N2O emissions are stimulated by NH4+ and NH2OH, respectively. Addition of 3,4-dimethylpyrazole phosphate (DMPP) and acetylene significantly reduced HONO and NOx emissions, while NH3 emissions were significantly enhanced in an alkaline Fluvo-aquic soil. These results suggested that ammonia-oxidizing bacteria (AOB) and complete ammonia-oxidizing bacteria (comammox Nitrospira) dominate HONO and NOx emissions in the alkaline Fluvo-aquic soil, while ammonia-oxidizing archaea (AOA) are dominant in the acidic Mollisol. DMPP effectively mitigated the warming effect in the Fluvo-aquic soil and the Ultisol. In conclusion, our findings highlight NO2- significantly stimulates HONO and NOx emissions from dryland agricultural soils, dominated by nitrification. In addition, subtle differences of soil NH3, N2O, HONO, and NOx emissions indicated different N turnover processes, and should be considered in biogeochemical and atmospheric chemistry models.