Formulation design and characterization of silymarin liposomes for enhanced antitumor activity.

Liposomes, a nanoscale carrier, plays an important role in the delivery of drug, affects the in vivo efficacy of drugs. In this paper, silymarin(SM)-loaded liposomes was optimized using the response surface method (RSM), with entrapment efficiency (EE%) as an index. The formulation was optimized as follow: lecithin (7.8mg/mL), SM/lecithin (1/26) and lecithin/cholesterol (10/1). The optimized SM liposomes had a high EE (96.58 ±3.06%), with a particle size of 290.3 ±10.5nm and a zeta potential of +22.98 ±1.73mV. In vitro release tests revealed that SM was released in a sustained-release manner, primarily via diffusion mechanism. In vitro cytotoxicity studies demonstrated that the prepared SM liposomes had stronger inhibitory effects than the model drug. Overall, these results indicate that this liposome system is suitable for intravenous delivery to enhance the antitumor effects of SM.

Correlation between NGS panel-based mutation results and clinical information in colorectal cancer patients.

Early mutation identification guides patients with colorectal cancer (CRC) toward targeted therapies. In the present study, 414 patients with CRC were enrolled, and amplicon-based targeted next-generation sequencing (NGS) was then performed to detect genomic alterations within the 73 cancer-related genes in the OncoAim panel. The overall mutation rate was 91.5 % (379/414). Gene mutations were detected in 38/73 genes tested. The most frequently mutated genes were TP53 (60.9 %), KRAS (46.6 %), APC (30.4 %), PIK3CA (15.9 %), FBXW7 (8.2 %), SMAD4 (6.8 %), BRAF (6.5 %), and NRAS (3.9 %). Compared with the wild type, TP53 mutations were associated with low microsatellite instability/microsatellite stability (MSI-L/MSS) (P = 0.007), tumor location (P = 0.043), and histological grade (P = 0.0009); KRAS mutations were associated with female gender (P = 0.026), distant metastasis (P = 0.023), TNM stage (P = 0.013), and histological grade (P = 0.004); APC mutations were associated with patients <64 years of age at diagnosis (P = 0.04); PIK3CA mutations were associated with tumor location (P = 4.97e-06) and female gender (P = 0.018); SMAD4 mutations were associated with tumor location (P = 0.033); BRAF mutations were associated with high MSI (MSI-H; P = 6.968e-07), tumor location (P = 1.58e-06), and histological grade (P = 0.04). Mutations in 164 individuals were found to be pathogenic or likely pathogenic. A total of 26 patients harbored MSI-H tumors and they all had at least one detected gene mutation. Mutated genes were enriched in signaling pathways associated with CRC. The present findings have important implications for improving the personalized treatment of patients with CRC in China.

Research on predicting hematoma expansion in spontaneous intracerebral hemorrhage based on deep features of the VGG-19 network.

PURPOSE: To construct a clinical noncontrastive computed tomography (NCCT) deep learning joint model for predicting early hematoma expansion (HE) after cerebral hemorrhage (sICH) and evaluate its predictive performance. METHODS: All 254 patients with primary cerebral hemorrhage from January 2017 to December 2022 in the General Hospital of the Western Theater Command were included. According to the criteria of hematoma enlargement exceeding 33% or the volume exceeding 6 ml, the patients were divided into the HE group and the hematoma non-enlargement (NHE) group. Multiple models and the 10-fold cross-validation method were used to screen the most valuable features and model the probability of predicting HE. The area under the curve (AUC) was used to analyze the prediction efficiency of each model for HE. RESULTS: They were randomly divided into a training set of 204 cases in an 8:2 ratio and 50 cases of the test set. The clinical imaging deep feature joint model (22 features) predicted the area under the curve of HE as follows: clinical Navie Bayes model AUC 0.779, traditional radiology logistic regression (LR) model AUC 0.818, deep learning LR model AUC 0.873, and clinical NCCT deep learning multilayer perceptron model AUC 0.921. CONCLUSION: The combined clinical imaging deep learning model has a high predictive effect for early HE in sICH patients, which is helpful for clinical individualized assessment of the risk of early HE in sICH patients.

Blockade of aryl hydrocarbon receptor restricts omeprazole-induced chronic kidney disease.

Chronic kidney disease (CKD) is the 16th leading cause of mortality worldwide. Clinical studies have raised that long-term use of omeprazole (OME) is associated with the morbidity of CKD. OME is commonly used in clinical practice to treat peptic ulcers and gastroesophageal reflux disease. However, the mechanism underlying renal failure following OME treatment remains mostly unknown and the rodent model of OME-induced CKD is yet to be established. We described the process of renal injury after exposure to OME in mice; the early renal injury markers were increased in renal tubular epithelial cells (RTECs). And after long-term OME treatment, the OME-induced CKD mice model was established. Herein, aryl hydrocarbon receptor (AHR) translocation appeared after exposure to OME in HK-2 cells. Then for both in vivo and in vitro, we found that Ahr-knockout (KO) and AHR small interfering RNA (siRNA) substantially alleviated the OME-induced renal function impairment and tubular cell damage. Furthermore, our data demonstrate that antagonists of AHR and CYP1A1 could attenuate OME-induced tubular cell impairment in HK-2 cells. Taken together, these data indicate that OME induces CKD through the activation of the AHR-CYP axis in RTECs. Our findings suggest that blocking the AHR-CYP1A1 pathway acts as a potential strategy for the treatment of CKD caused by OME. KEY MESSAGES: We provide an omeprazole-induced chronic kidney disease (CKD) mice model. AHR activation and translocation process was involved in renal tubular damage and promoted the occurrence of CKD. The process of omeprazole nephrotoxicity can be ameliorated by blockade of the AHR-CYP1A1 axis.

Bergamot essential oil improves CUMS-induced depression-like behaviour in rats by protecting the plasticity of hippocampal neurons.

Bergamot essential oil (BEO) is an extract of the bergamot fruit with significant neuroprotective effect. This study was to investigate the effects and the underlying mechanism of BEO in mitigating depression. GC-MS were used to identify its constituents. Antidepressive properties of BEO were evaluated by sucrose preference test (SPT), force swimming test (FST) and open field test (OFT). Nissl staining was used to determine the number of Nissl bodies in hippocampus (HIPP) of rats. Changes in HIPP dendritic length and dendritic spine density were detected by Golgi-Cox staining. Immunohistochemistry and Western blot were used to detect the postsynaptic density protein-95 (PSD-95) and synaptophysin (SYP) in the HIPP of rats. The enzyme-linked immunosorbent assay was used to determine the 5-hydroxytryptamine (5-HT), insulin-like growth factor 1 (IGF-1) and interleukin-1ß (IL-1ß) in the HIPP, serum and cerebrospinal fluid (CSF) of rats. Inhaled BEO significantly improved depressive behaviour in chronic unpredictable mild stress (CUMS) rats. BEO increased Nissl bodies, dendritic length and spine density, PSD-95 and SYP protein in the HIPP. Additionally, BEO upregulated serum 5-HT, serum and CSF IGF-1, while downregulating serum IL-1ß. Collectively, inhaled BEO mitigates depression by protecting the plasticity of hippocampal neurons, hence, providing novel insights into treatment of depression.

Elevated expression of Toll-like receptor 7 and its correlation with clinical features in patients with primary Sjögren's syndrome.

BACKGROUND: The labial salivary glands (LSGs) are important for the diagnosis, evaluation of therapeutic efficacy, and genetic analyses of primary Sjögren's syndrome (pSS). In autoimmune diseases, the recognition of self nucleic acids and viral RNA and DNA through endogenous Toll-like receptor(TLR) triggers the production of type I IFN and pro-inflammatory cytokines, leading to the occurrence and progression of the disease. Here, we detected the expression of TLR7 in LSGs and analyse its correlation with clinical features and serum cytokines in pSS patients. METHODS: LSGs and serum samples were obtained from 56 pSS patients and 19 non-SS patients (non-pSS patients). The expression of TLR7 in the LSGs was evaluated with immunohistochemistry. The serum levels of interferon-α (IFN-α) and interleukin-6 (IL-6) were quantified by ELISA. Laboratory parameters were measured by clinical standard laboratory techniques. RESULTS: TLR7-positive cells in pSS were localized in the ductal epithelial cells and lymphocytes of LSGs. The expression of TLR7 was upregulated in pSS patients compared with controls. Patients with anti-Ro52 antibody positivity showed higher TLR7 levels than those who were negative but not those with anti-Ro60 and anti-SSB. TLR7 levels were positively associated with the levels of IgG, IgA, ANA, IL-6, IFN-α and serum globulin but were not associated with IgM, C3, C4, or rheumatoid factor (RF) in serum. CONCLUSION: TLR7 may be involved in the inflammatory response and the production of antibodies in pSS and plays an important role in local and systemic pSS manifestations. This research showed that TLR7 is involved in pSS pathogenesis.

Correlation between genetic alterations and clinicopathological features of papillary thyroid carcinomas.

OBJECTIVE: To investigate the correlations between multigene alterations and clinicopathological features in papillary thyroid carcinoma (PTC) samples. METHODS: In this retrospective study, 111 cytological specimens of thyroid nodules, including 74 PTC samples and 37 benign samples, were analyzed using a 22-gene mutation assay employing next-generation sequencing. Clinicopathological information was retrospectively collected and analyzed. RESULTS: Gene alterations were associated with a higher rate of lymph node metastasis (LNM) and thyroid capsular invasion, a lower rate of coexisting Hashimoto's thyroiditis, the classical PTC subtype, and younger age (<45 years). Among the 22 genes tested, the BRAF mutation rates showed a significant difference between the PTC and benign groups. In the subgroup analysis, younger age (odds ratio = 12.512, 95% confidence interval: 3.126-50.087) was an independent risk factor for LNM. In further analyses, BRAF mutation was significantly associated with LNM in the older subgroup (age ≥ 45 years), suggesting that the BRAF mutation test has greater value for determining PTC prognosis in the older age group. CONCLUSIONS: Our findings will provide a more comprehensive understanding of the relationship between gene mutations and PTC and may contribute to improved PTC management.

High Response and Selectivity of the SnO2 Nanobox Gas Sensor for Ethyl Methyl Carbonate Leakage Detection in a Lithium-Ion battery.

It is well-known that metal-oxide semiconductors (MOS) have significant gas sensing activity and are widely used in harmful gas monitoring in various environments. With the rapid development of new energy vehicles, the monitoring of the gas composition and concentration in LIB has become an effective way to avoid safety problems. However, the study of typical electrolyte solvent detection, such as EMC and DMC detection by the MOS sensor, is still in its infancy. Here, the SnO2 nanoboxes are synthesized by coordination dissolution using cubic Cu2O as the template, and its sensor shows high sensitivity (0.27 to 10 ppb EMC), excellent response (32.46 to 20 ppm EMC), and superior selectivity. Additionally, the sensor possesses fast and clear response to lithium-ion battery (LIB) leakage simulation tests, suggesting that it should be a promising candidate for LIB safety monitors. These sensing performances are attributed to large specific surface area, small grain size, and high size/thickness ratio of nanoboxes. More importantly, DFT calculations confirm the adsorption of EMC on the surface of the SnO2 nanoboxes, and the EMC decomposition processes catalyzed by SnO2 are deduced by in situ FTIR and GC-MS.

Development of an Intratumoral and Peritumoral Radiomics Nomogram Using Digital Breast Tomosynthesis for Preoperative Assessment of Lymphovascular Invasion in Invasive Breast Cancer.

RATIONALE AND OBJECTIVES: This study aimed to create a nomogram model that combines clinical factors with radiomics analysis of both intra- and peritumoral regions extracted from preoperative digital breast tomosynthesis (DBT) images, in order to develop a reliable method for predicting the lymphovascular invasion (LVI) status in invasive breast cancer (IBC) patients. MATERIALS AND METHODS: A total of 178 patients were randomly split into a training dataset (N = 124) and a validation dataset (N = 54). Comprehensive clinical data, encompassing DBT features, were gathered for all cases. Radiomics features were extracted and selected from intra- and peritumoral region to establish radiomics signature (Radscore). To construct the clinical model and nomogram model, univariate and multivariate logistic regression analyses were utilized to identify independent risk factors. To assess and validate these models, various analytical methods were employed, including receiver operating characteristic (ROC) curve analysis, calibration curve analysis, decision curve analysis (DCA), net reclassification improvement (NRI), and integrated discriminatory improvement (IDI). RESULTS: The clinical model is constructed based on two independent risk factors: tumor margin and the DBT-reported lymph node metastasis (DBT_reported_LNM). Incorporating Radscore_Combine (utilizing both intra- and peritumoral radiomics features), tumor margin, and DBT_reported_LNM into the nomogram achieved a reliable predictive performance, with area under the curve (AUC) values of 0.906 and 0.905 in both datasets, respectively. The significant improvement demonstrated by the NRI and IDI indicates that the Radscore_Combine could be a valuable biomarker for effectively predicting the status of LVI. CONCLUSION: The nomogram demonstrated a reliable ability to predict LVI in IBC patients.

Upregulation of Parkinson's disease-associated protein alpha-synuclein suppresses tumorigenesis via interaction with mGluR5 and gamma-synuclein in liver cancer.

Numerous epidemiological studies suggest a link between Parkinson's disease (PD) and cancer, indicating that PD-associated proteins may mediate the development of cancer. Here, we investigated a potential role of PD-associated protein α-synuclein in regulating liver cancer progression in vivo and in vitro. We found the negative correlation of α-synuclein with metabotropic glutamate receptor 5 (mGluR5) and γ-synuclein by analyzing the data from The Cancer Genome Atlas database, liver cancer patients and hepatoma cells with overexpressed α-synuclein. Moreover, upregulated α-synuclein suppressed the growth, migration, and invasion. α-synuclein was found to associate with mGluR5 and γ-synuclein, and the truncated N-terminal of α-synuclein was essential for the interaction. Furthermore, overexpressed α-synuclein exerted the inhibitory effect on hepatoma cells through the degradation of mGluR5 and γ-synuclein via α-synuclein-dependent autophagy-lysosomal pathway (ALP). Consistently, in vivo experiments with rotenone-induced rat model of PD also confirmed that, upregulated α-synuclein in liver cancer tissues through targeting on mGluR5/α-synuclein/γ-synuclein complex inhibited tumorigenesis involving in ALP-dependent degradation of mGluR5 and γ-synuclein. These findings give an insight into an important role of PD-associated protein α-synuclein accompanied by the complex of mGluR5/α-synuclein/γ-synuclein in distant communications between PD and liver cancer, and provide a new strategy in therapeutics for the treatment of liver cancer.

A fluorene derivative inhibits human hepatocellular carcinoma cells by ROS-mediated apoptosis, anoikis and autophagy.

Fluorene was previously reported to have anticancer activity against human cancer cells. In this study, we examined the in vitro function of 9-methanesulfonylmethylene-2, 3-dimethoxy-9 H -fluorene (MSDF), a novel fluorene derivative, its anticancer potential in human hepatocellular carcinoma (HCC) cells and its underlying molecular mechanism. The disruption of cellular homeostasis caused by MSDF was found to promote reactive oxygen species (ROS) generation, leading to the activation of cellular apoptosis. As a survival strategy, cells undergo autophagy during oxidative stress. MSDF-induced apoptosis occurred through both receptor-mediated extrinsic and mitochondrial-mediated intrinsic routes. The development of acidic vesicular organelles and the accumulation of LC3-II protein suggest an increase in the autophagic process. Apoptosis was detected by double staining. The MAPK/ERK and PI3K/Akt signaling pathways were indeed suppressed during treatment. Along with elevated ROS generation and apoptosis, MSDF also caused anoikis and cell death by causing cells to lose contact with their extracellular matrix. ROS production was induced by MSDF and sustained by an NAC scavenger. MSDF-induced apoptosis led to increased autophagy, as shown by the suppression of apoptosis by Z-VAD-FMK. However, inhibition of autophagy by inhibitor 3-MA increased MSDF-induced apoptosis. More evidence shows that MSDF downregulated the expression of immune checkpoint proteins, suggesting that MSDF could be used in the future as an adjuvant to improve the effectiveness of HCC immunotherapy. Altogether, our results highlight the potential of MSDF as a multitarget drug for the treatment of HCC.

Cytosine arabinoside exposure induced cytotoxic effects and neural tube defects in mice and embryo stem cells.

Cytosine arabinoside (Ara-C) is one of the most widely used chemotherapeutic agents for hematological malignancies. The residues of Ara-C have been detected in wastewater and river water with increased usage and discharge. As the ability to cross the placenta and the teratogenicity at low ng/L levels, the toxic effects on pregnant women and infants have been concerned. The toxicity of Ara-C exposure on early embryonic neurodevelopment has not been fully elucidated. In this study, pregnant C57BL/6 mice were injected with different doses of Ara-C on Gestation day (GD) 7.5 and assessed on GD11.5 and GD13.5 to explore the neural developmental effects of Ara-C. HE staining, immunofluorescence, western blot, EdU assay, and flow cytometry were utilized to determine the toxic effects of Ara-C in vivo and in vitro. Our results showed that Ara-C (15-22.5 mg/kg body weight) induced the occurrence of neural tube defects (NTDs). The expression of PH3 was markedly reduced in embryos with Ara-C-induced NTDs, compared to the control group (P < 0.05). In contrast, cell apoptosis was markedly increased. Increased expression levels of GFAP and decreased Nestin were observed in the embryonic brain tissues in Ara-C induced NTDs. The level of ß-catenin was also decreased on both GD11.5 and GD13.5. These results were confirmed in vitro using mouse Sv129 embryonic stem cells (mESC). Ara-C at a dose comparable to the environment level (0.05 nM) had cytotoxicity. Impaired Wnt/ß-catenin signaling pathway is involved in Ara-C exposure induced imbalance between cell proliferation, apoptosis, and differentiation, which might contribute to Ara-C-induced occurrence of NTDs. Our data indicated the environmental concentration of Ara-C had cytotoxicity and that maternal exposure to Ara-C induced NTDs. These results might provide more information to understand the environmental toxic impact of Ara-C on neurodevelopment.

The Parkinson's disease-associated protein α-synuclein inhibits hepatoma by exosome delivery.

Numerous epidemiological studies suggest a link between Parkinson's disease (PD) and cancer. However, their relevant pathogenesis is not clear. In the present study, we investigated the potential role of exosome-delivered α-synuclein (α-syn) in the regulation between PD and liver cancer. We cultured hepatocellular carcinoma (HCC) cells with exosomes derived from conditioned medium of the PD cellular model, and injected exosomes enriched with α-syn into the striatum of a liver cancer rat model. We found that α-syn-contained exosomes from the rotenone-induced cellular model of PD suppressed the growth, migration, and invasion of HCC cells. Integrin αVß5 in exosomes from the rotenone-induced PD model was higher than that in the control, resulting in more α-syn-contained exosomes being taken up by HCC cells. Consistently, in vivo experiments with rat models also confirmed exosome-delivered α-syn inhibited liver cancer. These findings illustrate the important role of PD-associated protein α-syn inhibiting hepatoma by exosome delivery, suggesting a new mechanism underlying the link between these two diseases and therapeutics of liver cancer.

Radiomics nomogram based on digital breast tomosynthesis: preoperative evaluation of axillary lymph node metastasis in breast carcinoma.

PURPOSE: This study aimed to establish a radiomics nomogram model based on digital breast tomosynthesis (DBT) images, to predict the status of axillary lymph nodes (ALN) in patients with breast carcinoma. METHODS: The data of 120 patients with confirmed breast carcinoma, including 49 cases with axillary lymph node metastasis (ALNM), were retrospectively analyzed in this study. The dataset was randomly divided into a training group consisting of 84 patients (37 with ALNM) and a validation group comprising 36 patients (12 with ALNM). Clinical information was collected for all cases, and radiomics features were extracted from DBT images. Feature selection was performed to develop the Radscore model. Univariate and multivariate logistic regression analysis were employed to identify independent risk factors for constructing both the clinical model and nomogram model. To evaluate the performance of these models, receiver operating characteristic (ROC) curve analysis, calibration curve, decision curve analysis (DCA), net reclassification improvement (NRI), and integrated discriminatory improvement (IDI) were conducted. RESULTS: The clinical model identified tumor margin and DBT_reported_LNM as independent risk factors, while the Radscore model was constructed using 9 selected radiomics features. Incorporating tumor margin, DBT_reported_LNM, and Radscore, the radiomics nomogram model exhibited superior performance with AUC values of 0.933 and 0.920 in both datasets, respectively. The NRI and IDI showed a significant improvement, suggesting that the Radscore may serve as a useful biomarker for predicting ALN status. CONCLUSION: The radiomics nomogram based on DBT demonstrated effective preoperative prediction performance for ALNM in patients with breast cancer.

Adsorption of chitosan combined with nicotinamide-modified eupatorium adenophorum biochar to Sb3+: Application of DFT calculation.

The pollution and harm of Sb3+ to aquatic systems is a global problem, so Sb3+ removal from the water environment to make sure environment safety and human beings wellbeing is of urgency. This study explored the effect of chitosan combined with nicotinamide-modified eupatorium adenophorum biochar (CEBC) on adsorbing Sb3+ through batch adsorption experiments. The experiments indicated CEBC's maximum adsorption capacity to Sb3+ is 170.15 mg·g-1. Meanwhile, the capacity of the original biochar (EBC) is only 9.97 mg·g-1. Compared with EBC, CEBC contains more functional groups, such as CO, -OH and -NH2. In addition, the pseudo-second-order kinetic model and the Langmuir model are fit to describe the kinetics and isotherms of adsorption of CEBC to Sb3+, which suggests that the adsorption of CEBC to Sb3+ is dominated by monolayer chemisorption. Density functional theory (DFT) calculations confirmed that the chelation between -NH2 and Sb3+ is of significance in the adsorption process of CEBC. DFT calculations also found that the newly added -OH and CO in EBC have a synergistic enhancement effect on the absorption of Sb3+. The mechanism of CEBC absorbing Sb3+ includes electrostatic interactions, pore filling, Л-Л interactions, hydrogen bonding, functional group complexation, chelation, and oxidation. CEBC has an excellent anti-interference ability for inorganic anions (NO3-, SO42- and Cl-) and can also use the coexisting HA to improve its adsorption performance. In addition, CEBC has better mitigation of Sb3+ on the performance of Sb3+ about its secondary release and good reproducibility, which indicates that CEBC is a viable Sb3+ adsorbent.

Recent progress in nickel-catalyzed carboboration of alkenes.

Alkenes represent one of the most useful building blocks for organic synthesis, owing to their abundance and versatile reactivity. Transition metal (Pd, Cu, Co, Ni, Fe, etc.) catalyzed difunctionalization of alkenes provides efficient access to substituted molecules from readily available alkenes by installing functional groups across their carbon-carbon double bonds. Particularly, Nickel-based catalytic complexes have attracted a great deal of attention. This is because they are prone to undergoing oxidative addition and slow ß-hydride elimination, and can access both two-electron and radical pathways. Numerous elegant Ni-catalyzed cross-coupling methods, e.g., (hetero)arylboration, alkenylboration, alkylboration and alkynylboration of alkenes, have been developed with broad scopes and a high tolerance to a variety of functional groups. Therefore, the Ni-catalyzed carboboration of alkenes has become an efficient synthetic protocol to deliver substituted compounds by the cross-coupling of alkenes, electrophiles, and B2Pin2. Despite this progress, a number of challenging issues remaining in the field include broadening the types of carboboration reactions, especially the asymmetric ones, diversifying electrophile types (which is limited to halogens for now) and gaining profound insight into the reaction mechanisms. This review summarizes the recent progress in this emerging field from the literature published since 2018. It will provide the scientific community with convenience to access collective information and to accelerate their further research in order to broaden the scope of methodology and application in drug discovery programs.

Synthesis, determination, and bio-application in cellular and biomass-bamboo imaging of natural cinnamaldehyde derivatives.

Cinnamon essential oil (CEO) is the main ingredient in the renewable biomass of cinnamon, which contains natural cinnamaldehyde. To valorize the value of cinnamaldehyde, two simple and useful compounds (1 and 2) from CEO were synthesized using a Schiff-base reaction and characterized by infrared spectra (IR), nuclear magnetic resonance (NMR), and high-resolution mass spectrometry (HRMS). Compound 1 was used to confirm the presence of Fe3+ and ClO- in solution, as well as compound 2. Using fluorescence enhancement phenomena, it offered practicable linear relationship of 1's fluorescence intensity and Fe3+ concentrations: (0-8.0 × 10-5 mol/L), y = 36.232x + 45.054, R 2 = 0.9947, with a limit of detection (LOD) of 0.323 µM, as well as compound 2. With increasing fluorescence, F404/F426 of 1 and the ClO- concentration (0-1.0 × 10-4 mol/L) also had a linear relationship: y = 0.0392x + 0.5545, R 2 = 0.9931, LOD = 0.165 µM. However, the fluorescence intensity of 2 (596 nm) was quenched by a reduced concentration of ClO-, resulting in a linear. In addition, compounds 1 and 2 were used to image human astrocytoma MG (U-251), brain neuroblastoma (LN-229) cells, and bamboo tissue by adding Fe3+ or ClO-, with clear intracellular fluorescence. Thus, the two compounds based on CEO could be used to dye cells and bamboo tissues by fluorescence technology.

Association of Householder Smoking With Poverty and the Mediating Effect of NCDs in Relatively Underdeveloped Regions in China.

Background: Studies have not provided clear enough evidence on the direct association between cigarette smoking and poverty. This study aims to assess the association of householder smoking with near-poverty households, and the potential mediating effect of NCDs. Methods: A cross-sectional survey was conducted from November 2019 to October 2020 in relatively underdeveloped regions in China. In total, 2,409 households were investigated in areas under the jurisdiction of 24 primary health care (PHC) institutions of eight provinces. Pearson's χ2-test was performed, and multivariable logistic regression and extended probit regression models were fitted to examine the association between householder smoking and near-poverty households. Moreover, generalized structural equation modeling was used to explore the mediating effect of NCDs. Results: After adjusting for all other potential confounding factors, compared with households headed by never-smokers, households headed by smokers exhibited significantly elevated risks of being near poverty, with an odds ratio of 2.01 (95% CI: 0.48-0.91). We also found that living in rural areas and having a low education level both had a negative effect on being near poverty. Additionally, NCDs had a significantly positive mediating effect, with a 31.57% effect of householder smoking on near-poverty status mediated by NCDs; the indirect effect was estimated to be 0.17 (95% CI: 0.04-0.31). Conclusions: Householder smoking significantly elevated the risk of the household being near poverty, and suffering NCDs had a positive mediating effect.