Effects of Water Isotope Composition on Stable Isotope Distribution and Fractionation of Rice and Plant Tissues.

Rice origin authenticity is important for food safety and consumer confidence. The stable isotope composition of rice is believed to be closely related to its water source, which affects its origin characteristics. However, the influence of water availability on the distribution of rice stable isotopes (δ2H and δ18O) is not clear. In this study, three irrigation waters with different isotopic values were used to investigate isotopic water use effects of Indica and Japonica rice, using pot experiments. Under three different water isotope treatments, the δ2H values of Indica polished rice showed significant differences (-65.0 ± 2.3, -60.5 ± 0.8 and -55.8 ± 1.7‰, respectively, p < 0.05) compared to δ13C and δ15N, as did Japonica polished rice. The values of δ2H and δ18O of rice became more positive when applying more enriched (in 2H and 18O) water, and the enrichment effect was higher in rice than in the corresponding plant tissue. In addition, the δ2H and δ18O values of Indica rice leaves decreased at the heading stage, increased at the filling stage, and then decreased at the harvest stage. Japonica rice showed a similar trend. δ2H changes from stem to leaf were more negative, but δ18O changes were more positive, and δ2H and δ18O values from leaf to rice were more positive for both brown and polished rice. The results from this study will clarify different water isotopic composition effects on rice and provide useful information to improve rice origin authenticity using stable isotope-based methods.

Global trade-driven transfer of atmospheric polycyclic aromatic hydrocarbon emissions and associated human inhalation exposure risk.

Polycyclic aromatic hydrocarbons (PAHs) are of significant public concern because of their toxicity and long-range transport potential. Extensive studies have been conducted to explore the source-receptor relationships of PAHs via atmospheric transport. However, the transfer of trade-driven regional and global PAHs is poorly understood. This study estimated the virtual PAHs emission transfer embodied in global trade from 2004 to 2014 and simulated the impact of international trade on global contamination and associated human inhalation exposure risk of PAHs. Results show that trade-driven PAHs flowed primarily from developed to less-developed regions, particularly in those regions with intensive heavy industries and transportation. As the result, international trade resulted in an increasing risk of lung cancer induced by exposure to PAHs (27.8% in China, 14.7% in India, and 11.3% in Southeast Asia). In contrast, we found decreasing risks of PAHs-induced lung cancer in Western Europe (63.2%) and the United States (45.9%) in 2004. Our findings indicate that final demand and emission intensity are the key driving factors contributing to rising and falling consumption-based PAHs emissions and related health risk respectively. The results could provide a useful reference for global collaboration in the reduction of PAHs pollution and related health risks.

A study on short-term efficacy and safety of Iodine-125 brachytherapy coupled with preoperative arterial chemoembolization for hypervascular spinal metastasis.

PURPOSE: Hypervascular spinal metastatic malignancies can cause severe pain and intraoperative bleeding and selection of appropriate treatment can be challenging. This study aimed to observe the short-term efficacy and safety of Iodine-125 brachytherapy (125I BT) combined with preoperative transcatheter arterial chemoembolization (TACE) for hypervascular spinal metastasis. METHODS: This study included a total of 33 patients (39 lesions) with hypervascular spinal metastasis. All of them carried out a regimen of TACE followed by 125I BT under CT guidance. A brachytherapy planning system has been utilized for the purpose of designing treatment plans and optimizing dose distribution. Pain relief was evaluated using a numeric rating scale (NRS) and intraoperative bleeding was recorded. Follow-up was conducted for 6 months to observe the local control rate and clinical complications. RESULTS: All patients tolerated combined treatment well and intraoperative blood loss of every patient was not more than 10 ml. The 2- and 6- month local disease control rates were 92.3% and 83.8%. The NRS scores for thirty-three tumor patients before surgery and after one week, two, and six months of surgery were recorded as 7.33 ± 1.80, 7.39 ± 1.89, 3.15 ± 2.35, and 4.16 ± 2.15, respectively. The NRS score 2 months after treatment was found considerably lower in comparison to the NRS score before operation (p < 0.05). CONCLUSIONS: According to our findings, 125I BT as well as preoperative TACE leads to perioperative hemostasis, pain alleviation, and reduced tumor burden, indicating that this combined treatment could be effective and promising for hypervascular spinal metastases.

Foxj3 Regulates Thermogenesis of Brown and Beige Fat Via Induction of PGC-1α.

Enhancing the development of and thermogenesis in brown and beige fat represents a potential treatment for obesity. In this study, we show that Foxj3 expression in fat is stimulated by cold exposure and a ß-adrenergic agonist. Adipose-specific Foxj3 knockout impaired the thermogenic function of brown fat, leading to morphological whitening of brown fat and obesity. Adipose Foxj3-deficient mice displayed increased fasting blood glucose levels and hepatic steatosis while on a chow diet. Foxj3 deficiency inhibited the browning of inguinal white adipose tissue (iWAT) following ß3-agonist treatment of mice. Furthermore, depletion of Foxj3 in primary brown adipocytes reduced the expression of thermogenic genes and cellular respiration, indicating that the Foxj3 effects on the thermogenic program are cell autonomous. In contrast, Foxj3 overexpression in primary brown adipocytes enhanced the thermogenic program. Moreover, AAV-mediated Foxj3 overexpression in brown fat and iWAT increased energy expenditure and improved systemic metabolism on either a chow or high-fat diet. Finally, Foxj3 deletion in fat inhibited the ß3-agonist-mediated induction of WAT browning and brown adipose tissue thermogenesis. Mechanistically, cold-inducible Foxj3 stimulated the expression of PGC-1α and UCP1, subsequently promoting energy expenditure. This study identifies Foxj3 as a critical regulator of fat thermogenesis, and targeting Foxj3 in fat might be a therapeutic strategy for treating obesity and metabolic diseases.

Mid-infrared dual-comb spectroscopy for rapid temperature distribution characterization.

Due to the influence of chemical reactions, phase change, and other phenomena, the combustion system is a complicated high-temperature environment. Therefore, the spatio-temporally resolved monitoring of the temperature field is crucial for gaining a comprehensive understanding of the intricate combustion environment. In this study, we proposed a fast and high-precision temperature measurement technique based on mid-infrared (MIR) dual-comb spectroscopy with a high spectral resolution and fast refresh rate. Based on this technique, the spatio-temporally resolved measurement of a non-uniform temperature field was achieved along the laser path. To verify the capability of DCS for temperature measurement, the bandhead ro-vibrational lines of the CO2 molecule were acquired, and the 1-σ uncertainty of the retrieved temperature was 3.2°C at 800°C within 100 ms. The results demonstrate the potential of our fast and high-precision laser diagnostic technique which can be further applied to combustion kinetics.

A selective CB2R agonist (JWH133) protects against pulmonary fibrosis through inhibiting FAK/ERK/S100A4 signaling pathways.

BACKGROUND: The combination of the endocannabinoid system (ECS) and the type 2 cannabinoid receptor (CB2R) can activate various signal pathways, leading to distinct pathophysiological roles. This interaction has gained significant attention in recent research on fibrosis diseases. Focal adhesion kinase (FAK) plays a crucial role in regulating signals from growth factor receptors and Integrins. It is also involved in the transformation of fibroblasts into myofibroblasts. This study aims to investigate the impact of the CB2R agonist JWH133 on lung fibrosis and its potential to alleviate pulmonary fibrosis in mice through the FAK pathway. METHODS: The C57 mice were categorized into five groups: control, BLM, BLM + JWH133, BLM + JWH133 + NC, and BLM + JWH133 + FAK groups.JWH133 was administered to mice individually or in conjunction with the FAK vector. After 21 days, pathological changes in mouse lung tissues, inflammatory factor levels, hydroxyproline levels, and collagen contents were evaluated. Moreover, the levels of the FAK/ERK/S100A4 pathway-related proteins were measured. RESULTS: JWH133 treatment decreased inflammatory factor levels, attenuated pathological changes, and reduced extracellular matrix accumulation in the mouse model of bleomycin-induced pulmonary fibrosis; however, these effects were reversed by FAK. JWH133 attenuated fibrosis by regulating the FAK/ERK/S100A4 pathway. CONCLUSIONS: The results presented in this study show that JWH133 exerts a protective effect against pulmonary fibrosis by inhibiting the FAK/ERK/S100A4 pathway.Therefore, JWH133 holds promise as a potential therapeutic target for pulmonary fibrosis.

Temperature-dependent determination of NO2 dimerization reaction based on dual-comb spectroscopy.

Dimerization reactions play a critical role in various fields of research, including cell biology, biomedicine, and chemistry. In particular, the dimerization reaction of 2NO2⇌N2O4 has been extensively applied in pollution control and raw material preparation. Spectroscopy, as a powerful tool for investigating molecular structures and reaction kinetics, has been increasingly employed to study dimerization reactions in recent years. In this study, we successfully demonstrated the application of dual-comb spectroscopy (DCS) to analyze NO2 dimerization reactions, making the first report on the application of this technique in this context. Parallel measurements of NO2 and N2O4 fingerprints spectra with high resolution at 3000 cm-1 was performed, benefiting from the unprecedented broadband and high-precision capability of DCS. The absorption cross-sections of N2O4 from 296 to 343 K was obtained from the measured spectra, which contributes to further research on the molecular spectrum of N2O4. These results demonstrate the potential of DCS for studying the dimerization reaction mechanism.

Lower subcutaneous fat index predicts bone metastasis in breast cancer.

BACKGROUND: Bone metastases affect 50% to 70% of breast cancer (BC) patients and have a high mortality rate. Adipose tissue loss plays a pivotal role in the progression of cancer. OBJECTIVE: This study aims to evaluate the prognostic value of adipose tissue for bone metastasis in BC patients. METHODS: 517 BC patients were studied retrospectively. Patients' characteristics before the surgery were collected. Quantitative measurements of the subcutaneous fat index (SFI) were performed at the level of the eleventh thoracic vertebra. In order to adjust for the heterogeneity between the low SFI and high SFI groups, propensity score matching (PSM) was used. The Kaplan-Meier method was used to estimate the 5-year bone metastatic incidence. The prognostic analysis was performed with the Cox regression models. RESULTS: Compared with the patients without bone metastasis, the patients with bone metastasis had reduced SFI levels. In addition, Kaplan-Meier analysis revealed that patients with low SFI were more likely to develop bone metastases. The independent predictive value of SFI for bone metastases was confirmed by Cox regression analysis. The survival analysis was repeated after PSM with a 1:1 ratio, yielding similar results (P< 0.05). CONCLUSIONS: SFI is an independent predictor of bone metastasis in BC patients.

Amifostine attenuates bleomycin-induced pulmonary fibrosis in mice through inhibition of the PI3K/Akt/mTOR signaling pathway.

Amifostine is a normal cell protection agent, not only used in the adjuvant therapy of lung cancer, ovarian cancer, breast cancer, nasopharyngeal cancer, bone tumor, digestive tract tumor, blood system tumor and other cancers in order to reduce the toxicity of chemotherapy drugs, and recent studies have reported that the drug can also reduce lung tissue damage in patients with pulmonary fibrosis, but its mechanism of action is not yet fully understood. In this study, we explored the potential therapeutic effects and molecular mechanisms of AMI on bleomycin (BLM)-induced pulmonary fibrosis in mice. A mouse model of pulmonary fibrosis was established using BLM. We then assessed histopathological changes, inflammatory factors, oxidative indicators, apoptosis, epithelial-mesenchymal transition, extracellular matrix changes, and levels of phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway-related proteins in the BLM-treated mice to determine the effect of AMI treatment on these factors. BLM-treated mice had substantial lung inflammation and abnormal extracellular matrix deposition. Overall, treatment with AMI significantly improved BLM-induced lung injury and pulmonary fibrosis. More specifically, AMI alleviated BLM-induced oxidative stress, inflammation, alveolar cell apoptosis, epithelial-mesenchymal transition, and extracellular matrix deposition by regulating the PI3K/Akt/mTOR signaling pathway. This finding that AMI can alleviate pulmonary fibrosis in a mouse model by inhibiting activation of the PI3K/Akt/mTOR signaling pathway lays a foundation for potential future clinical application of this agent in patients with pulmonary fibrosis.

Nintedanib Ameliorates Bleomycin-Induced Pulmonary Fibrosis, Inflammation, Apoptosis, and Oxidative Stress by Modulating PI3K/Akt/mTOR Pathway in Mice.

Idiopathic pulmonary fibrosis (IPF) seriously threatens human life and health, and no curative therapy is available at present. Nintedanib is the first agent approved by the US Food and Drug Administration (FDA) in order to treat IPF; however, its mechanism of inhibition of IPF is still elusive. According to recent studies, nintedanib is a potent inhibitor. It can antagonize platelet-derived growth factor (PDGF), basic fibroblast growth factor (b-FGF), vascular endothelial growth factor (VEGF), etc., to inhibit pulmonary fibrosis. Whether there are other signaling pathways involved in IPF remains unknown. This study focused on investigating the therapeutic efficacy of nintedanib in bleomycin-mediated pulmonary fibrosis (PF) mice through PI3K/Akt/mTOR pathway. Following the induction of pulmonary fibrosis in C57 mice through bleomycin (BLM) administration, the mice were randomized into five groups: (1) the normal control group, (2) the BLM model control group, (3) the low-dose Nintedanib administration model group, (4) the medium-dose nintedanib administration model group, and (5) the high-dose nintedanib administration model group. For lung tissues, morphological changes were found by HE staining and Masson staining, ELISA method was used to detect inflammatory factors, alkaline water method to estimate collagen content, and western blotting for protein levels. TUNEL staining and immunofluorescence methods were used to analyze the effect of nintedanib on lung tissue and the impacts and underlying mechanisms of bleomycin-induced pulmonary fibrosis. After 28 days, bleomycin-treated mice developed significant pulmonary fibrosis. Relative to bleomycin-treated mice, nintedanib-treated mice had markedly reduced degrees of PF. In addition, nintedanib showed lung-protective effects by up-regulating antioxidant levels, down-regulating inflammatory protein expression, and reducing collagen accumulation. We demonstrated that nintedanib ameliorated bleomycin-induced lung injury by inhibiting the P13K/Akt/mTOR pathway as well as apoptosis. In addition, significant improvement in pulmonary fibrosis was seen after nintedanib (30/60/120 mg/kg body weight/day) treatment through a dose-dependent way. Histopathological results further corroborated the effect of nintedanib treatment on remarkably attenuating bleomycin-mediated mouse lung injury. According to our findings, nintedanib restores the antioxidant system, suppresses pro-inflammatory factors, and inhibits apoptosis. Nintedanib can reduce bleomycin-induced inflammation by downregulating PI3K/Akt/mTOR pathway, PF, and oxidative stress (OS).

Air pollution and associated health impact and economic loss embodied in inter-provincial electricity transfer in China.

As the largest producer and consumer of coal in the world, China heavily relies on coal resources for thermal power generation. Owing to the unbalanced distribution of energy resources, electricity transfer among regions in China plays a key role in promoting economic growth and ensuring energy safety. However, little is known about air pollution and the related health impacts resulting from electricity transfer. This study assessed PM2.5 pollution and related health and economic losses attributable to the inter-provincial electricity transfer in mainland China in 2016. The results show that a large amount of virtual air pollutant emissions were transferred from energy-abundant northern, western and central China to well-developed and populated eastern coastal regions. Correspondingly, the inter-provincial electricity transfer dramatically reduced the atmospheric levels of PM2.5 and related health and economic losses in eastern and southern China, while increasing those in northern, western and central China. The health benefits attributable to inter-provincial electricity transfer were mainly found in Guangdong, Liaoning, Jiangsu and Shandong, whereas the extra health loss is concentrated in Hebei, Shanxi, Inner Mongolia, and Heilongjiang. Overall, the inter-provincial electricity transfer led to an extra increase of 3600 (95 % CI: 3200-4100) PM2.5-related deaths and 345 (95 % CI: 294-389) million USD of economic loss in China in 2016. The results could assist air pollution mitigation strategies for the thermal power sector in China by strengthening the cooperation between suppliers and consumers of electricity.

Comprehensive analysis of an endoplasmic reticulum stress-related gene prediction model and immune infiltration in idiopathic pulmonary fibrosis.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease. This study aimed to investigate the involvement of endoplasmic reticulum stress (ERS) in IPF and explore its correlation with immune infiltration. Methods: ERS-related differentially expressed genes (ERSRDEGs) were identified by intersecting differentially expressed genes (DEGs) from three Gene Expression Omnibus datasets with ERS-related gene sets. Gene Set Variation Analysis and Gene Ontology were used to explore the potential biological mechanisms underlying ERS. A nomogram was developed using the risk signature derived from the ERSRDEGs to perform risk assessment. The diagnostic value of the risk signature was evaluated using receiver operating characteristics, calibration, and decision curve analyses. The ERS score of patients with IPF was measured using a single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm. Subsequently, a prognostic model based on the ERS scores was established. The proportion of immune cell infiltration was assessed using the ssGSEA and CIBERSORT algorithms. Finally, the expression of ERSRDEGs was validated in vivo and in vitro via RT-qPCR. Results: This study developed an 8-ERSRDEGs signature. Based on the expression of these genes, we constructed a diagnostic nomogram model in which agouti-related neuropeptide had a significantly greater impact on the model. The area under the curve values for the predictive value of the ERSRDEGs signature were 0.975 and 1.000 for GSE70866 and GSE110147, respectively. We developed a prognostic model based on the ERS scores of patients with IPF. Furthermore, we classified patients with IPF into two subtypes based on their signatures. The RT-qPCR validation results supported the reliability of most of our conclusions. Conclusion: We developed and verified a risk model using eight ERSRDEGs. These eight genes can potentially affect the progression of IPF by regulating ERS and immune responses.

Nintedanib alleviates pulmonary fibrosis in vitro and in vivo by inhibiting the FAK/ERK/S100A4 signalling pathway.

Nintedanib is an effective treatment for pulmonary fibrosis (PF), but the exact mechanism by which this agent works to delay the progression of PF remains unclear. In this study, we explored whether nintedanib alleviates PF at least partially by inhibiting the focal adhesion kinase (FAK)/ERK/S100A4 signalling pathway. Bleomycin (BLM) was used to induce PF in a mouse model, and human fetal lung fibroblast 1 (HFL-1) cells were exposed to transforming growth factor-ß 1 (TGF-ß1) to create an in vitro model of PF. In both models, nintedanib was administered either alone or in conjunction with a FAK vector. In mouse lung tissues, histopathology, inflammatory factor levels, and collagen content were assessed; in HFL-1 cells, HFL-1 activity was assessed, along with collagen I, collagen III, and α-SMA levels. Both mouse tissue and HFL-1 cells were examined for levels of indices associated with extracellular matrix and the FAK/ERK/S100A4 signalling pathway. In mice exposed to BLM, lung inflammation and extracellular matrix deposition were significantly increased. These factors were alleviated by nintedanib treatment but were aggravated by overexpression of FAK. In HFL-1 cells, nintedanib inhibited HFL-1 activity and collagen I, collagen III, and α-SMA levels, whereas overexpression of FAK produced the opposite effect. In both tissues and cells, the FAK/ERK/S100A4 signalling pathway was activated, but nintedanib was able to suppress this pathway. These results suggest that nintedanib alleviates PF by inhibiting the FAK/ERK/S100A4 signalling pathway both in vivo and in vitro.

Preoperative PDW levels predict pulmonary metastasis in patients with hepatocellular carcinoma.

BACKGROUND: In hepatocellular carcinoma (HCC), pulmonary metastasis (PM) after hepatectomy is associated with poor clinical outcomes. The crucial phases of tumour cell proliferation, angiogenesis, and metastasis all entail platelet activation. In HCC, platelet distribution width (PDW) suggests platelet size changes and predicts a worse prognosis. The aim of this study was to assess the association between PDW and PMs in HCC patients receiving hepatectomy. MATERIAL/METHODS: From January 2013 to December 2015, a cohort of patients who underwent hepatectomy for HCC at the Harbin Medical University Cancer Hospital in China were retrospectively evaluated. The relationship between PDW levels and clinical and demographic parameters was examined. To investigate the relationships between predicted factors and PM, a competing risk model was used. From January 2016 to December 2018, a validation cohort of 109 patients from the First Affiliated Hospital of Harbin Medical University was studied independently. RESULTS: In the primary cohort, 19 out of 214 patients had postoperative PMs. In HCC patients with PM, PDW levels were lower than in those without PM. There was a significant difference in the cumulative incidence of 2-year PM between the high-PDW and low-PDW groups after controlling for competing risk events (death prior to the development of PM) (p < 0.001). In addition, PDW was also found to be an independent predictor for PM in a multivariable competing risk analysis. The results were externally validated in another cohort. CONCLUSIONS: In HCC, preoperative PDW is significantly associated with PM. PDW could be a biomarker for post-operative PM in HCC patients.

Utility of mean platelet volume in differentiating intrahepatic cholangiocarcinoma from hepatocellular carcinoma.

BACKGROUND: Intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC) are the most prevalent histologic types of primary liver cancer. HCC and ICC differ in treatment and prognosis, warranting an effective differential diagnosis between them. This study aimed to explore the clinical value of mean platelet volume (MPV) to discriminate between HCC and ICC. MATERIAL/METHODS: We performed a retrospective analysis of ICC and HCC patients who were from the Harbin Medical University Cancer Hospital, China. Logistic regression analysis was used to identify the independent factors for the differentiation of HCC and ICC. A receiver operating characteristic curve was built to evaluate the diagnostic performance of the potential model. An independent validation study was performed to validate the diagnostic ability. RESULTS: ICC patients were detected in 146 out of 348 patients in the primary cohort. MPV levels were decreased in ICC patients compared with those in HCC patients. Logistic regression analysis revealed that MPV was an independent factor in distinguishing HCC from ICC. A combination of sex, hepatitis B surface antigen, MPV, alpha-fetoprotein, and carbohydrate antigen 19-9 demonstrated a good capability to differentiate HCC from ICC. Similar results were achieved in the validation cohort. CONCLUSIONS: MPV may be a new marker to help distinguish ICC from HCC. Further validation studies are required.

Preoperative Pectoralis Muscle Index Predicts Distant Metastasis-Free Survival in Breast Cancer Patients.

Background: Breast cancer is one of the most commonly diagnosed cancers, and the fourth leading cause of cancer deaths in females worldwide. Sarcopenia is related to adverse clinical outcomes in patients with malignancies. Muscle index is a key parameter in evaluating sarcopenia. However, there is no data investigating the association between muscle index and distant metastasis in breast cancer. The aim of this study was to explore whether muscle index can effectively predict distant metastasis and death outcomes in breast cancer patients. Study Design: The clinical data of 493 breast cancer patients at the Harbin Medical University Cancer Hospital between January 2014 and December 2015 were retrospectively analyzed. Quantitative measurements of pectoralis muscle area and skeletal muscle area were performed at the level of the fourth thoracic vertebra (T4) and the eleventh thoracic vertebra (T11) of the chest computed tomography image, respectively. The pectoralis muscle index (PMI) and skeletal muscle index (SMI) were assessed by the normalized muscle area (area/the square of height). Survival analysis was performed using the log-rank test and Cox proportional hazards regression analysis. Result: The patients with metastases had lower PMI at T4 level (PMI/T4) and SMI at T11 level (SMI/T11) compared with the patients without metastases. Moreover, there were significant correlations between PMI/T4 and lymphovascular invasion, Ki67 expression, multifocal disease, and molecular subtype. In addition, multivariate analysis revealed that PMI/T4, not SMI/T11, was an independent prognostic factor for distant metastasis-free survival (DMFS) and overall survival (OS) in breast cancer patients. Conclusions: Low PMI/T4 is associated with worse DMFS and OS in breast cancer patients. Future prospective studies are needed.

FGF9 Alleviates the Fatty Liver Phenotype by Regulating Hepatic Lipid Metabolism.

Although the fatty liver has been linked to numerous impairments of energy homeostasis, the molecular mechanism responsible for fatty liver development remains largely unknown. In the present study, we show that fibroblast growth factors 9 (FGF9) expression is increased in the liver of diet-induced obese (DIO), db/db, and ob/ob mice relative to their respective controls. The long-term knockdown of hepatic FGF9 expression mediated by adeno-associated virus expressing FGF9-specific short hairpin RNA (AAV-shFGF9) aggravated the fatty liver phenotype of DIO mice. Consistently, downregulation of FGF9 expression mediated by adenovirus expressing FGF9-specific shRNA (Ad-shFGF9) in the primary hepatocyte promoted the cellular lipid accumulation, suggesting that FGF9 exerts its effects in an autocrine manner. In contrast, adenoviruses expressing FGF9 (Ad-FGF9) mediated FGF9 overexpression in the liver of DIO mice alleviated hepatic steatosis and improved the insulin sensitivity and glucose intolerance. Moreover, the liver-specific FGF9 transgenic mice phenocopied the Ad-FGF9-infected mice. Mechanistically, FGF9 inhibited the expression of genes involved in lipogenesis and increased the expression of genes involved in fatty acid oxidation, thereby reducing cellular lipid accumulation. Thus, targeting FGF9 might be exploited to treat nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome.

Recent Progress Regarding Materials and Structures of Triboelectric Nanogenerators for AR and VR.

With the continuous advancement in technology, electronic products used in augmented reality (AR) and virtual reality (VR) have gradually entered the public eye. As a result, the power supplies of these electronic devices have attracted more attention from scientists. Compared to traditional power sources, triboelectric nanogenerators (TENGs) are gradually being used for energy harvesting in self-powered sensing technology such as wearable flexible electronics, including AR and VR devices due to their small size, high conversion efficiency, and low energy consumption. As a result, TENGs are the most popular power supplies for AR and VR products. This article first summarizes the working mode and basic theory of TENGs, then reviews the TENG modules used in AR and VR devices, and finally summarizes the material selection and design methods used for TENG preparation. The friction layer of the TENG can be made of a variety of materials such as polymers, metals, and inorganic materials, and among these, polytetrafluoroethylene (PTFE) and polydimethylsiloxane (PDMS) are the most popular materials. To improve TENG performance, the friction layer material must be suitable. Therefore, for different application scenarios, the design methods of the TENG play an important role in its performance, and a reasonable selection of preparation materials and design methods can greatly improve the work efficiency of the TENG. Lastly, we summarize the current research status of nanogenerators, analyze and suggest future application fields, and summarize the main points of material selection.

Online Shopping Brand Sales Based on IoT Big Data Processing.

As a pair of closely related technical fields, "Internet of Things" and "big data" are gradually applied to the analysis of online shopping, which is very beneficial to promote the healthy and orderly development of the online shopping industry. This article uses the big data processing technology of the Internet of Things to analyze the influencing factors of online shopping brand sales based on the data collected by online questionnaires. It draws certain rules from it, and provides relevant marketing strategies for online shopping brand sales to assist its market positioning. According to the survey, the five aspects of online evaluation, brand awareness, online shopping community, online public opinion influence of related brands, and other brand information acquisition channels all have an impact on online brand sales. Especially women aged 25-35 will pay attention to online information, and 195 people will not choose to buy from brands with negative news. And during the purchase process, 186 people will check the online reviews of related brand products. Among them, there are 183 men aged 25-35 who will pay attention to online reviews.

Transcription factor Klf9 controls bile acid reabsorption and enterohepatic circulation in mice via promoting intestinal Asbt expression.

Bile acid (BA) homeostasis is regulated by the extensive cross-talk between liver and intestine. Many bile-acid-activated signaling pathways have become attractive therapeutic targets for the treatment of metabolic disorders. In this study we investigated the regulatory mechanisms of BA in the intestine. We showed that the BA levels in the gallbladder and faeces were significantly increased, whereas serum BA levels decreased in systemic Krüppel-like factor 9 (Klf9) deficiency (Klf9-/-) mice. These phenotypes were also observed in the intestine-specific Klf9-deleted (Klf9vil-/-) mice. In contrast, BA levels in the gallbladder and faeces were reduced, whereas BA levels in the serum were increased in intestinal Klf9 transgenic (Klf9Rosa26+/+) mice. By using a combination of biochemical, molecular and functional assays, we revealed that Klf9 promoted the expression of apical sodium-dependent bile acid transporter (Asbt) in the terminal ileum to enhance BA absorption in the intestine. Reabsorbed BA affected liver BA synthetic enzymes by regulating Fgf15 expression. This study has identified a previously neglected transcriptional pathway that regulates BA homeostasis.