Evaluation of electromagnetic scattering characteristics of construction solid waste-A theoretical study of solid waste identification.

The surge in urban development has resulted in a substantial accumulation of construction solid waste (CSW). However, prevailing identification methods of CSW remain predominantly two-dimensional in scope and need to be more efficient. This study employs an approach, combining simulation and experimental analyses, to delve into the factors influencing the electromagnetic scattering characteristics of CSW, investigating the feasibility of employing Synthetic Aperture Radar (SAR) to recognize CSW. The findings show that the computational time of MLFMM and PO is only 3.28 % and 0.029 % of MM among different simulation methods. The results underscore the collective impact of material types, surface structures, and curvature on the scattering characteristics of CSW. The difference in average intensity between different materials can reach up to 13 dB. Exploiting these distinctions in scattering enables the precise identification of high-value waste components, such as intact bricks and steel bars, within the intricate landscape of CSW.

Genetic variant in a BaP-activated super-enhancer increases prostate cancer risk by promoting AhR-mediated FAM227A expression.

Genetic variants in super-enhancers (SEs) are increasingly implicated as a disease risk-driving mechanism. Previous studies have reported an associations between benzo[a]pyrene (BaP) exposure and some malignant tumor risk. Currently, it is unclear whether BaP is involved in the effect of genetic variants in SEs on prostate cancer risk, nor the associated intrinsic molecular mechanisms. In the current study, by using logistic regression analysis, we found that rs5750581T>C in 22q-SE was significantly associated with prostate cancer risk (odds ratio = 1.26, P = 7.61 × 10 -5). We also have found that the rs6001092T>G, in a high linkage disequilibrium with rs5750581T>C ( r 2 = 0.98), is located in a regulatory aryl hydrocarbon receptor (AhR) motif and may interact with the FAM227A promoter in further bioinformatics analysis. We then performed a series of functional and BaP acute exposure experiments to assess biological function of the genetic variant and the target gene. Biologically, the rs6001092-G allele strengthened the transcription factor binding affinity to AhR, thereby upregulating FAM227A, especially upon exposure to BaP, which induced the malignant phenotypes of prostate cancer. The current study highlights that AhR acts as an environmental sensor of BaP and is involved in the SE-mediated prostate cancer risk, which may provide new insights into the etiology of prostate cancer associated with the inherited SE variants under environmental carcinogen stressors.

Rapid dataset generation methods for stacked construction solid waste based on machine vision and deep learning.

The development of urbanization has brought convenience to people, but it has also brought a lot of harmful construction solid waste. The machine vision detection algorithm is the crucial technology for finely sorting solid waste, which is faster and more stable than traditional methods. However, accurate identification relies on large datasets, while the datasets from the field working conditions are scarce, and the manual annotation cost of datasets is high. To rapidly and automatically generate datasets for stacked construction waste, an acquisition and detection platform was built to automatically collect different groups of RGB-D images for instances labeling. Then, based on the distribution points generation theory and data augmentation algorithm, a rapid-generation method for synthetic construction solid waste datasets was proposed. Additionally, two automatic annotation methods for real stacked construction solid waste datasets based on semi-supervised self-training and RGB-D fusion edge detection were proposed, and datasets under real-world conditions yield better models training results. Finally, two different working conditions were designed to validate these methods. Under the simple working condition, the generated dataset achieved an F1-score of 95.98, higher than 94.81 for the manually labeled dataset. In the complicated working condition, the F1-score obtained by the rapid generation method reached 97.74. In contrast, the F1-score of the dataset obtained manually labeled was only 85.97, which demonstrates the effectiveness of proposed approaches.

Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease.

As a recently discovered waste removal system in the brain, cerebral lymphatic system is thought to play an important role in regulating the homeostasis of the central nervous system. Currently, more and more attention is being focused on the cerebral lymphatic system. Further understanding of the structural and functional characteristics of cerebral lymphatic system is essential to better understand the pathogenesis of diseases and to explore therapeutic approaches. In this review, we summarize the structural components and functional characteristics of cerebral lymphatic system. More importantly, it is closely associated with peripheral system diseases in the gastrointestinal tract, liver, and kidney. However, there is still a gap in the study of the cerebral lymphatic system. However, we believe that it is a critical mediator of the interactions between the central nervous system and the peripheral system.

Exploring the Utilization of PHC Pile Waste Concrete as Filler in Asphalt Mastics.

Using solid waste to replace limestone filler in asphalt concrete can not only reduce the cost of road construction, but also improve the utilization rate of solid waste. In this study, PHC pile waste concrete (PPWC) was innovatively used to replace limestone filler in asphalt mixture and its effect on the physical and rheological properties of asphalt mastics was studied. Firstly, PPWC was ground into filler particles with a diameter less than 0.075 mm. The physical properties, particle characteristics and chemical composition of PPWC filler and limestone filler were compared. Asphalt mastics were prepared with different filler-asphalt volume ratios (20%, 30% and 40%) and the physical properties, high-temperature rheological properties and low-temperature cracking resistance of asphalt mastics were tested. The experimental results showed that the surface of PPWC filler is rougher and has lower density and smaller particle size than limestone filler. When the filler content is the same, PPWC filler asphalt mastics have lower penetration and ductility, higher softening point than limestone filler asphalt mastics, and the viscosity of PPWC filler asphalt mastics is more sensitive than limestone filler asphalt mastics. PPWC filler asphalt mastics demonstrated superior high-temperature stability, but poorer low-temperature cracking resistance compared to limestone filler asphalt mastics. In conclusion, PPWC fillers can be used to replace limestone fillers in asphalt mixtures. The finding of this study will provide a new solution for the construction of eco-friendly roads.

In Vitro Anti-Tumor and Hypoglycemic Effects of Total Flavonoids from Willow Buds.

Salix babylonica L. is a species of willow tree that is widely cultivated worldwide as an ornamental plant, but its medicinal resources have not yet been reasonably developed or utilized. Herein, we extracted and purified the total flavonoids from willow buds (PTFW) for component analysis in order to evaluate their in vitro anti-tumor and hypoglycemic activities. Through Q-Orbitrap LC-MS/MS analysis, a total of 10 flavonoid compounds were identified (including flavones, flavan-3-ols, and flavonols). The inhibitory effects of PTFW on the proliferation of cervical cancer HeLa cells, colon cancer HT-29 cells, and breast cancer MCF7 cells were evaluated using an MTT assay. Moreover, the hypoglycemic activity of PTFW was determined by investigating the inhibitory effects of PTFW on α-amylase and α-glucosidase. The results indicated that PTFW significantly suppressed the proliferation of HeLa cells, HT-29 cells, and MCF7 cells, with IC50 values of 1.432, 0.3476, and 2.297 mg/mL, respectively. PTFW, at different concentrations, had certain inhibitory effects on α-amylase and α-glucosidase, with IC50 values of 2.94 mg/mL and 1.87 mg/mL, respectively. In conclusion, PTFW at different doses exhibits anti-proliferation effects on all three types of cancer cells, particularly on HT-29 cells, and also shows significant hypoglycemic effects. Willow buds have the potential to be used in functional food and pharmaceutical industries.

Role of NAT10-mediated ac4C-modified HSP90AA1 RNA acetylation in ER stress-mediated metastasis and lenvatinib resistance in hepatocellular carcinoma.

Emerging evidence showed that epigenetic regulation plays important role in the pathogenesis of HCC. N4-acetocytidine (ac4C) was an acetylation chemical modification of mRNA, and NAT10 is reported to regulate ac4C modification and enhance endoplasmic reticulum stress (ERS) in tumor metastasis. Here, we report a novel mechanism by which NAT10-mediated mRNA ac4C-modified HSP90AA1 regulates metastasis and tumor resistance in ERS of HCC. Immunohistochemical, bioinformatics analyses, and in vitro and in vivo experiments, e.g., acRIP-Seq, RNA-Seq, and double luciferase reporter experiment, were employed to investigate the effect of NAT10 on metastasis and drug resistance in HCC. The increased expression of NAT10 was associated with HCC risk and poor prognosis. Cell and animal experiments showed that NAT10 enhanced the metastasis ability and apoptosis resistance of HCC cells in ERS and ERS state. NAT10 could upregulate the modification level of HSP90AA1 mRNA ac4C, maintain the stability of HSP90AA1, and upregulate the expression of HSP90AA1, which further promotes the metastasis of ERS hepatoma cells and the resistance to apoptosis of Lenvatinib. This study proposes a novel mechanism by which NAT10-mediated mRNA ac4C modification regulates tumor metastasis. In addition, we demonstrated the regulatory effect of NAT10-HSP90AA1 on metastasis and drug resistance of ERS in HCC cells.

Tastin promotes non-small-cell lung cancer progression through the ErbB4, PI3K/AKT, and ERK1/2 pathways.

Tastin might be involved in tumorigenesis, but its role in non-small-cell lung cancer (NSCLC) has not been adequately explored. This work aimed to examine tastin's role in NSCLC and to explore the underlying mechanism. The Gene Expression Omnibus (GEO), Gene Expression Database of Normal and Tumor tissues (GENT), and Cancer Genome Atlas (TCGA) databases were used. Four GEO datasets (GSE81089, GSE40419, GSE74706, and GSE19188) containing gene expression data for NSCLC and normal tissue samples were analyzed for tastin mRNA expression. Tastin expression levels in different tissues were compared using the GENT website. TCGA biolinks were used to download gene expression quantification (n = 594) and overall survival data (n = 535). In total, 30 lung adenocarcinoma and 25 lung squamous cell carcinoma cases were enrolled. In addition, four-week-old male BALB/c nude mice (n = 9/group) were used to establish xenograft mouse models. Furthermore, cultured HEK293T, A549, and NCI-H226 cells assessed. Immunoblot, hematoxylin and eosin (H&E) staining, immunohistochemistry, real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), fluorescence microscopy, flow cytometry, lentiviral transduction, and MTT, colony formation, wound healing, and Transwell assays were carried out. Tastin expression levels were markedly increased in NSCLC tumor tissue specimens and correlated with a poorer prognosis. Silencing of tastin inhibited the proliferative and migratory abilities of NSCLC cells. Bioinformatic analysis suggested that tastin interacts with ErbB4. The PI3K/AKT and ERK1/2 downstream pathways were suppressed in tastin-deficient cells. In conclusion, tastin might be involved in NSCLC growth and invasion and is a potential therapeutic target in NSCLC.

Conversion mechanism of thermal plasma-enhanced CH4-CO2 reforming system to syngas under the non-catalytic conditions.

Thermal plasma activation of CH4-CO2 reforming (CRM) to syngas under non-catalytic conditions is an efficient and clean technology for the large-scale utilization of hydrocarbon resources and the conversion of greenhouse gases. This study investigates the equilibrium state and transformation mechanism of a CRM reaction system activated by thermal plasma through experimental, thermodynamic, and kinetic analyses. The experimental results illustrated that the CO2 conversion rate and H2 selectivity showed a downward trend with an increase in the CO2/CH4 molar ratio, whereas the CH4 conversion rate and CO selectivity showed the opposite trend. When CO2/CH4 molar ratio was 6/4, the selectivity for CO and H2 increased to 87.0 % and 80.8 %, respectively. Excess CO2 promotes the partial oxidation of CH4 to eliminate carbon deposition, resulting in an H2/CO molar ratio value closer to 1. Thermodynamic results show that the thermal-plasma-initiated CRM reaction can reach thermodynamic equilibrium more easily than the conventional catalyzed reactions, achieving much higher feedstock gas conversion without carbon deposition. The kinetic results obtained from the PSR model revealed that CH4 and CO2 were cleaved to form free radicals at the instant of contact with the plasma flame. O, H, and other particles generated in the form of free radicals rapidly collided with each other and transformed into CO and H2, accelerating the reaction process. The results presented in this study will help reveal the transformation mechanism of the CRM reaction activated by thermal plasma under non-catalytic conditions and provide a new perspective for studying CRM reactions.

Exosomal NAMPT from chronic lymphocytic leukemia cells orchestrate monocyte survival and phenotype under endoplasmic reticulum stress.

Endoplasmic reticulum (ER) stress has been reported to be transmitted from tumor cells to immune cells via exosome and implicated in immune escape. However, the influence of ER stress on monocytes in chronic lymphocytic leukemia (CLL) cells is largely unknown. Here, we observed the expression of ER stress markers (GRP78, ATF6, PERK, IRE1a, and XBP1s) in CLL cells. The increasing mRNA expression of these ER stress response components was positively correlated with more aggressive disease. Exosome from ER stress inducer tunicamycin (TM)-primed CLL cells (ERS-exo) up-regulated the expression of ER stress marker on monocytes, indicating ER stress is transmissible in vitro via exosome. Treatment with ERS-exo promoted the survival of monocytes and induced phenotypic changes with a significantly larger percentage of CD14+ CD16+ monocytes. Finally, we identified exosome-mediated transfer of extracellular nicotinamide phosphoribosyltransferase (eNAMPT) from ER stressed CLL cells into monocytes as a novel mechanism through which ERS-exo regulated monocytes. Exosomal eNAMPT up-regulated nicotinamide adenine dinucleotide (NAD+ ) production which subsequently activated SIRT1-C/EBPß signaling pathway in monocytes. Our results suggest the role of ER stress in mediating immunological dysfunction in CLL.

The Improvement of Sepsis-Associated Encephalopathy by P2X7R Inhibitor through Inhibiting the Omi/HtrA2 Apoptotic Signaling Pathway.

The pathogenesis of sepsis-associated encephalopathy (SAE) involves many aspects, including intracellular peroxidative stress damage, mitochondrial dysfunction, and cell apoptosis. In this study, we mainly explored the influence of P2X7R on the cognitive function of SAE and its molecular mechanism. We established a sepsis model using lipopolysaccharide (LPS) stimulation, followed by an assessment of cognitive function using Morris water maze, and then Western Blot was used to analyze the expression of tight junction proteins ZO-1 and Occludin in the hippocampus of mice. TUNEL assay was used to analyze the apoptosis of brain cells in frozen brain slices of mice during sepsis. Human brain microvascular endothelial cells (HBMECs) were used to research the molecular mechanism of brain cell damage induced by P2X7R. The results showed that P2X7R inhibitors dramatically improved the survival rate of mice, relieved the cognitive dysfunction caused by LPS stimulation, and significantly reduced the brain cell apoptosis caused by LPS. In addition, the inhibition of P2X7R can also reduce the production and accumulation of reactive oxygen species (ROS) in HBMECs in vitro and inhibit the apoptosis signaling pathway associated with mitochondrial serine protease Omi/HtrA2 in HBMECs in vitro. These results suggest that P2X7R has strong value as a potential target for the treatment of SAE.

RGB-D fusion models for construction and demolition waste detection.

The development of urbanization has brought a large amount of construction and demolition waste (CDW), which occupy land and cause adverse ecological effects. To effectively solve the negative impact of CDW, it needs to be recycled. Accurate waste classification is key to successful waste management. However, the current waste classification methods mainly use color images to classify, which cannot meet the needs of accurate classification. This paper built an RGB-depth (RGB-D) detection platform, using a color camera and a laser line-scanning sensor to collect RGB images and depth images. In order to use RGB images and depth images for feature fusion more effectively, this paper proposed three fusion models: RGB-D concat、RGB-D Ci-add and RGB-D Ci-concat. All these models based on an instance segmentation network called mask region convolutional neural network (Mask R-CNN), which can accurately segment the contours of each object while classifying them. The experimental results show that the mAPs of the RGB-D Ci-add / concat model are 1.33% to 1.72% higher than those of the RGB model, and the classification accuracy is 1.92% ∼ 2.27% higher. In addition, all the proposed models can meet the real-time requirement of online detection. Due to the excellent comprehensive performance of the RGB-D Ci-concat model, it can be regarded as the final detection model of the robot, which can improve the sorting efficiency of CDW further.

Intraoperative use of low-dose dexmedetomidine for the prevention of emergence agitation following general anaesthesia in elderly patients: a randomized controlled trial.

OBJECTIVE: To clarify the effect of an intraoperative low-dose dexmedetomidine infusion on emergence agitation following general anaesthesia in elderly patients. METHODS: Eighty elderly patients (> 64-years-old) following elective general anaesthesia for radical cancer surgeries were randomly allocated into two groups (n = 40 each): the dexmedetomidine group (Group D) and the normal saline group (Group C). Anaesthesia was maintained with continuous intravenous infusion of dexmedetomidine at - 0.2 µg kg-1 h-1 in Group D, and an equal volume of normal saline (0.5 ml kg-1 h-1) was given in Group C. All patients were observed for 30 min in the post-anaesthesia care unit (PACU), AFPS and NRS were recorded every 2 min, and the total doses of nalbuphine and fentanyl were calculated in the PACU. MAP and HR were recorded at the time of 10 min (T1), 20 min (T2), 30 min (T3) after dexmedetomidine or saline pumping, and before extubation (T4), immediately after extubation (T5), and 5 min after extubation (T6). We also documented some durations, including anaesthesia duration (D1), surgery duration (D2), duration from the end of surgery to extubation (D3), and emergence agitation duration (D4). RESULTS: The MAP in Group C was significantly higher than that in Group D (P < 0.05), and there were no significant changes between the two groups in HR and MAP within each time point and D1, D2, D3, and D4. The incidence of agitation, NRS score and total dose of nalbuphine and fentanyl were all lower in Group D than in Group C (P < 0.05). CONCLUSION: An intraoperative low-dose dexmedetomidine continuous infusion can reduce emergence agitation following general anaesthesia in elderly patients (> 64-years-old), remain stable in terms of haemodynamics, and not lead to delays in anaesthesia recovery time and extubation time.

Endoplasmic reticulum stress promotes sorafenib resistance via miR-188-5p/hnRNPA2B1-mediated upregulation of PKM2 in hepatocellular carcinoma.

Emerging evidence has shown that endoplasmic reticulum (ER) stress promotes sorafenib resistance in hepatocellular carcinoma (HCC). However, the underlying mechanisms are poorly understood. The purpose of this study was to explore the mechanism by which ER stress promotes sorafenib resistance in HCC. We found that pyruvate kinase isoform M2 (PKM2) was highly expressed in human HCC tissues and co-related with worse clinicopathologic features and overall survival. Activation of ER stress positively correlated with PKM2 expression both in HCC tissue samples and tunicamycin (TM)-induced HCC cell lines. PKM2 knockdown increased sorafenib-induced apoptosis and decreased the ability of colony formation, while upregulation of PKM2 reverses this phenomenon. Furthermore, high-throughput sequencing identified that activation of ER stress significantly downregulated the expression of miR-188-5p in HCC cells. According to bioinformatics analysis and dual-luciferase assays, we further confirmed that hnRNPA2B1 is the target gene of miR-188-5p. Downregulating the expression of hnRNPA2B1 with siRNA could decrease the expression of PKM2 and enhance sorafenib-induced apoptosis in HepG2 cells. Our study demonstrated that ER stress could promote sorafenib resistance through upregulating PKM2 via miR-188-5p/hnRNPA2B1. Therefore, targeting the miR-188-5p/hnRNPA2B1/PKM2 pathway and ER stress may prove instrumental in overcoming sorafenib resistance in HCC treatment.

The biogenesis and biological function of PIWI-interacting RNA in cancer.

Small non-coding RNAs (ncRNAs) are vital regulators of biological activities, and aberrant levels of small ncRNAs are commonly found in precancerous lesions and cancer. PIWI-interacting RNAs (piRNAs) are a novel type of small ncRNA initially discovered in germ cells that have a specific length (24-31 nucleotides), bind to PIWI proteins, and show 2'-O-methyl modification at the 3'-end. Numerous studies have revealed that piRNAs can play important roles in tumorigenesis via multiple biological regulatory mechanisms, including silencing transcriptional and posttranscriptional gene processes and accelerating multiprotein interactions. piRNAs are emerging players in the malignant transformation of normal cells and participate in the regulation of cancer hallmarks. Most of the specific cancer hallmarks regulated by piRNAs are involved in sustaining proliferative signaling, resistance to cell death or apoptosis, and activation of invasion and metastasis. Additionally, piRNAs have been used as biomarkers for cancer diagnosis and prognosis and have great potential for clinical utility. However, research on the underlying mechanisms of piRNAs in cancer is limited. Here, we systematically reviewed recent advances in the biogenesis and biological functions of piRNAs and relevant bioinformatics databases with the aim of providing insights into cancer diagnosis and clinical applications. We also focused on some cancer hallmarks rarely reported to be related to piRNAs, which can promote in-depth research of piRNAs in molecular biology and facilitate their clinical translation into cancer treatment.

A zinc finger family protein, ZNF263, promotes hepatocellular carcinoma resistance to apoptosis via activation of ER stress-dependent autophagy.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. Endoplasmic reticulum stress (ERS) is generally activated in HCC and is important for the sensitivity of HCC to anticancer drugs. ERS-dependent autophagy is a crucial mechanism affecting the sensitivity of HCC to anticancer drugs, but the mechanism by which ERS regulates autophagy is not well understood. Zinc finger protein 263 (ZNF263) is a transcription factor member of the zinc finger family. However, its functional role in HCC remains to be studied. In the current study, we investigated the role of ZNF263 in regulating ERS-induced chemoresistance in HCC and its possible mechanism. We found that ZNF263 was the most significant ERS-specific super-enhancer bounding transcriptional factor and was up-regulated in HCC patients and cell lines. Further, ZNF263 expression correlated with ERS, clinical stage and shorter survival in HCC patients. ZNF263 knockdown by RNA interference results in decreased proliferation, apoptosis resistance, and chemoresistance. Further study showed that ZNF263 increased chemoresistance by activating ERS-related autophagy. In conclusion, our study highlights ZNF263 as a functional ERS-related tumor activator and indicates it as a potential target for HCC therapy.

Overexpression of Rictor protein and Rictor-H. pylori interaction has impact on tumor progression and prognosis in patients with gastric cancer.

INTRODUCTION: Growing evidence indicates that Rictor (Rapamycin-insensitive companion of mTOR) is overexpressed across several malignancies and associated with poor survival. However, only limited data indicate that Rictor plays a role in gastric cancer (GC). We sought to explore the prognostic value of Rictor in GC and present interaction analysis between Rictor expression and H. pylori status regarding their effects over the prognosis of GC patient. MATERIALS AND METHODS: 250 GC tissues and 124 lymph node metastases were collected for the detection of Rictor by immunohistochemistry. Cox regression model was used to assess the association between Rictor expression and patient prognosis. Functional experiments were examined in transfected cells using Rictor siRNA. Additive and multiplicative interactions of Rictor and H. pylori were evaluated. RESULTS: In this study, the positive rate of Rictor was 51.6% (129/150) in GC tissues. Multivariate analyses showed that Rictor was independent unfavorable predictor for OS (HR = 1.554, 95% CI = 1.076-2.244, P = 0.019) and DFS (HR = 1.556, 95% CI = 1.081-2.240, P = 0.017). Patients with upregulated Rictor in the primary tumor and lymph node metastases had the worst prognosis. We observed significant additive and multiplicative interactions between Rictor expression and H. pylori status for OS and DFS (P < 0.05). Our in vitro experiment showed that knockdown of Rictor could suppress cell proliferation, induce apoptosis and inhibit tumor migration and invasion. CONCLUSION: Our results demonstrate that Rictor, acting as an oncogene, might be a potential prognostic biomarker and therapeutic target in GC. We suggest that Rictor expression and H. pylori status may be a prognostic marker in gastric cancer.

Exosomes derived from endoplasmic reticulum-stressed liver cancer cells enhance the expression of cytokines in macrophages via the STAT3 signaling pathway.

Previous studies have shown that endoplasmic reticulum (ER) stress serves an important role in shaping the immunosuppressive microenvironment by modulating resident immune cells. However, the communication between ER-stressed tumor cells and immune cells is not fully understood. Exosomes have been reported to play a vital role in intercellular communication. Therefore, in order to investigate the role of ER stress-related exosomes in liver cancer cells mediated macrophage function remodeling, immunohistochemical analysis, western-blotting immunofluorescence and cytokine bead array analyses were performed. The results demonstrated that glucose-regulated protein 78 (GRP78) expression was upregulated in human liver cancer tissue. Moreover, 69.09% of GRP78-positive liver cancer tissues possessed macrophages expressing CD68+ (r=0.55; P<0.001). In addition to these CD68+ macrophages, interleukin (IL)-10 and IL-6 expression levels were increased in liver cancer tissues. It was also demonstrated that exosomes released by ER-stressed HepG2 cells significantly enhanced the expression levels of several cytokines, including IL-6, monocyte chemotactic protein-1, IL-10 and tumor necrosis factor-α in macrophages. Furthermore, incubation of cells with ER stress-associated exosomes resulted inactivation of the Janus kinase 2/STAT3 pathway, and inhibition of STAT3 using S3I-201 in RAW264.7 cells significantly reduced cytokine production. Collectively, the present study identified a novel function of ER stress-associated exosomes in mediating macrophage cytokine secretion in the liver cancer microenvironment, and also indicated the potential of treating liver cancer via an ER stress-exosomal-STAT3 pathway.

Survival value of primary tumour resection for stage IV non-small-cell lung cancer: A population-based study of 6466 patients.

INTRODUCTION: For stage IV non-small-cell lung cancer (NSCLC) patients, surgical resection of primary tumour was rarely recommended. OBJECTIVES: We conducted this population-based study to demonstrate the survival value of primary tumour resection (PTR) for stage IV (NSCLC). METHODS: The Surveillance, Epidemiology and End Results (SEER) database was searched for selecting stage IV NSCLC patients. The patients were matched according to age, gender, grade, primary tumour site, histopathological type, tumour size and regional lymph nodes metastasis by propensity score matching (PSM) analysis. Kaplan-Meier curves were presented to show the survival differences between resection group and non-resection group. Risk factors which were supposed to influence survival outcome were investigated using a Cox proportional hazard regression model. And a nomogram was performed to present prognostic factors for stage IV NSCLC patients. RESULTS: 6466 patients diagnosed from 2004 to 2015 were included in survival analyses after PSM. The median overall survival (OS) for overall patients with resection was 27 months, much longer than those without resection (8 months). And this trend remained in subgroup analyses, including different histopathological types and distant metastases (All P values < 0.001). Younger age, race other than white and black, female, grade 1/2 (G1/G2), PTR, chemotherapy, no other distant metastases, smaller tumour size and no regional lymph node metastases were favourable prognostic factors for stage IV NSCLC. A predictive nomogram was conducted based on above risk factors. CONCLUSION: PTR prolonged survival of stage IV NSCLC patients. And PTR should be considered in clinical practice for stage IV NSCLC.

A study to evaluate herb-drug interaction underlying mechanisms: An investigation of ginsenosides attenuating the effect of warfarin on cardiovascular diseases.

Warfarin and ginseng have been widely used in the treatment of cardiovascular diseases. However, the clinical safety and effectiveness of herb-drug combination treatment are still controversial. Therefore, it is very essential to probe the interaction between warfarin and ginseng. In this study, in vitro and in vivo study was carried out to demonstrate that whether there is an interaction between warfarin and ginsenosides (GS), which is the main component of ginseng. In vitro study showed that the adhesion ability between endothelial cells and matrigel/platelets was enhanced due to the up-regulating expression of intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1) proteins by treatment of warfarin+GS combination compared to warfarin/GS treatment alone. Moreover, GS could weaken the anticoagulation effect of warfarin in hyperlipemia rats owning to the increased expression levels of coagulation factors and hepatic cytochrome P450 enzymes in plasma after long-term co-administration of warfarin with GS. The results of both in vitro and in vivo study demonstrated that there is a serious interaction between warfarin and ginseng, which may deteriorate atherosclerosis and thrombosis after combined use of warfarin and GS.