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Biliary stricture can be induced by intrinsic narrowing and extrinsic compression, with the majority of cases being malignant. Clinically, distinguishing between benign and malignant biliary strictures remains a considerable challenge, and the ongoing disagreement over the optimal choice of biliary stents significantly influences treatment strategies and impacts patients’ survival and prognosis. The utilization and advancement of endoscopic techniques have heightened the diagnostic sensitivity for biliary strictures. Concurrently, innovative technologies such as endoscopic ultrasound and magnetic compression anastomosis emerge as viable alternatives when endoscopic retrograde cholangiopancreatography (ERCP) is not an option, providing fresh insights for the clinical management of these patients. Traditional plastic and metal stents, characterized by their complex application and limited scope, have been unable to fully satisfy clinical needs. The introduction of novel stent varieties has notably improved this scenario, marking a considerable progression towards precision medicine. However, the clinical validation of the diverse stent materials available is incomplete. Hence, a thorough discussion on the present state and evolving trends of biliary stents is warranted.

Abstract Polymeric materials, rich in carbon, hydrogen, and oxygen elements, present substantial fire hazards to both human life and property due to their intrinsic flammability. Overcoming this challenge in the absence of any flame-retardant elements is a daunting task. Herein, we introduce an innovative strategy employing catalytic polymer auto-pyrolysis before combustion to proactively release CO2, akin to possessing responsive CO2 fire extinguishing mechanisms. We demonstrate that potassium salts with strong nucleophilicity (such as potassium formate/malate) can transform conventional polyurethane foam into materials with fire safety through rearrangement. This transformation results in the rapid generation of a substantial volume of CO2, occurring before the onset of intense decomposition, effectively extinguishing fires. The inclusion of just 1.05 wt% potassium formate can significantly raise the limiting oxygen index of polyurethane foam to 26.5%, increase the time to ignition by 927%, and tremendously reduce smoke toxicity by 95%. The successful application of various potassium salts, combined with a comprehensive examination of the underlying mechanisms, underscores the viability of this strategy. This pioneering catalytic approach paves the way for the efficient and eco-friendly development of polymeric materials with fire safety.

Abstract The rapidly increasing use of high-throughput screening had produced a plethora of expanding knowledge on the molecular basis of natural killer/T-cell lymphoma (NKTCL), which in turn has revolutionized the treatment. Specifically, the use of asparaginase-containing regimens has led to substantial improvement in survival outcomes in NKTCL patients. Novel treatment strategies that are currently under development include cell-surface-targeted antibodies, immune checkpoint inhibitors, Epstein-Barr virus targeted cytotoxic T lymphocyte, immunomodulatory agents, chimeric antigen receptor T cells, signaling pathway inhibitors and epigenetic targeted agents. In almost all cases, initial clinical studies of newly developed treatment are conducted in patients relapsed, and refractory NKTCL due to very limited treatment options. This review summarizes the results of these novel treatments for NKTCL and discusses their potential for likely use in NKTCL in a wider setting in the future.

This study constructs a model for the rapid identification of the origins of edible sunflower (Helianthus) using Kernel Extreme Learning Machine (KELM) with multi-source information fusion technology. Near-infrared spectroscopy (NIRS) and nuclear magnetic resonance spectroscopy (NMRS) were utilized to analyze 180 sunflower samples from the Xinjiang, Heilongjiang, and Inner Mongolia regions. Initially, the identification models for the origin of sunflowers using NIR and NMR data were compared between two algorithms: the Extreme Learning Machine (ELM) and KELM, combined with various spectral preprocessing methods. The experiment found that the NIR spectral model preprocessed with standard normal variate (SNV) using the KELM algorithm was the most accurate, achieving accuracies of 98.7% in the training set and 97.2% in the test set. The spin-echo NMR spectral model preprocessed with non-local means (NLMs) using the KELM algorithm was the second best, with accuracies of 98.4% in the training set and 96.4% in the test set. To further improve the accuracy of the identification models, innovative sunflower origin identification models were developed based on data layer fusion and feature layer fusion using NIRS and NMRS. In the data layer fusion model, the KELM algorithm model was optimal, achieving a test set accuracy and F1 score of 98.2% and 98.18%, respectively, an improvement of 1.0% over the best single data source model. In the feature layer fusion model, four types of feature-layer information-fusion identification models were established using two feature extraction algorithms, Competitive Adaptive Reweighted Sampling (CARS) and Variable Importance Projection (VIP), combined with joint feature and simple merging feature strategies. The CARS-KELM algorithm combined with the joint feature method was found to be the best, achieving 100% accuracy in both the training and test sets, an improvement of 2.8% over the best single data source model. Identifying the origin of edible sunflower using NIRS and NMRS is demonstrated as feasible by the results. The best single-spectrum sunflower origin identification model was achieved using the KELM algorithm with SNV preprocessing. The feature layer fusion method combining NIRS and NMRS data is suitable for handling the task of sunflower origin identification. This method significantly improves the recognition accuracy of the model compared to a single model, achieving fast and accurate origin identification of edible sunflowers. The research results provide a new method for rapid identification of sunflower origin.

This paper presents the background, scientific objectives, experimental design, and preliminary achievements of the Xin’anjiang nested experimental watershed (XAJ-NEW), implemented in 2017 in eastern China, which has a subtropical humid monsoon climate and a total area of 2674 km2. The scientific objectives of the XAJ-NEW include building a comprehensive, multiscale, and nested hydrometeorological monitoring and experimental program, strengthening the observation of the water cycle, discovering the spatiotemporal scaling effects of hydrological processes, and revealing the mechanisms controlling runoff generation and partitioning in a typical humid, hilly area. After two years of operation, preliminary results indicated scale-dependent variability in key hydrometeorological processes and variables such as precipitation, runoff, groundwater, and soil moisture. The effects of canopy interception and runoff partitioning between the surface and subsurface were also identified. Continuous operation of this program can further reveal the mechanisms controlling runoff generation and partitioning, discover the spatiotemporal scaling effects of hydrological processes, and understand the impacts of climate change on hydrological processes. These findings provide new insights into understanding multiscale hydrological processes and their responses to meteorological forcings, improving model parameterization schemes, and enhancing weather and climate forecast skills.

Introduction: The presence of hypoxic‐ischemic brain damage (HIBD) in neonates triggers a strong neuroinflammatory reaction. Pyroptosis, a programmed cell death mechanism associated with inflammation, plays a crucial role in HIBD. Pyruvate kinase M2 (PKM2) plays a significant role in connecting metabolic processes and inflammatory responses, but whether it affects hippocampus pyroptosis in HIBD is unclear. The aim of this study is to elucidate the role of PKM2 in HIBD and to propose a novel therapeutic approach for neonatal ischemic‐hypoxic encephalopathy. Methods: In this study, we employed neonatal 7‐day‐old Sprague Dawley rats to establish a model of HIBD using the Rice–Vannucci surgical technique and a hypoxia device. To inhibit the elevation of PKM2, we utilized the PKM2 inhibitor shikonin. The rats were categorized into four groups: Sham, Shikonin, HIBD, and Shikonin + HIBD. Behavioral tests, hematoxylin eosin staining, immunofluorescence staining, ELISA (IL‐1β, IL‐18), and LDH were conducted in each group to evaluate neurological function, hippocampal damage, the occurrence of neuronal pyroptosis, and the neuroinflammation. Western blot was used to assess the expression levels of PKM2, NLRP3, Caspase‐1, Cleaved Caspase‐1, GSDMD, GSDMDN, and IL‐1β. Results: The expression of PKM2 elevated in hippocampal tissues of the HIBD model and the localization of PKM2 in the hippocampus was activated in neurons instead of microglia during the HIBD. Meanwhile, the inhibition of PKM2 improved the behavioral test scores and the body weight of rats, the neuronal damage in the CA1 region of hippocampal tissue was also attenuated. In addition, inhibiting PKM2 alleviated neuronal pyroptosis by decreasing the expression of PKM2, NLRP3, Caspase‐1, Cleaved Caspase‐1, GSDMD, GSDMDN. Furthermore, serum levels of LDH and inflammatory factors IL‐1β and IL‐18 decrease with PKM2 inhibition. Conclusions: Based on these findings, we can conclude that PKM2 plays a crucial role in regulating hippocampal neuronal pyroptosis of HIBD rats via NLRP3/Caspase‐1/GSDMD pathway. Therefore, inhibiting PKM2 could be a promising therapeutic strategy for the treatment of neonatal ischemic‐hypoxic encephalopathy. [ABSTRACT FROM AUTHOR]

Pyroptosis is an inflammation‐associated programmed cell death, and neuroinflammation is strongly associated with severe neurological deficits in neonatal hypoxic–ischemic encephalopathy (HIE). Ethyl pyruvate (EP), a known anti‐inflammatory agent, has shown promise in the treatment of hypoxic–ischemic brain damage (HIBD) rats; nevertheless, the therapeutic mechanism of EP and its capacity to suppress neuronal pyroptosis in HIBD rats remain unclear. In both the neonatal Rice‐Vannucci rat model and the OGD/R model, this study examined alterations in the NLRP3/Caspase‐1/GSDMD classical pyroptosis pathway in hippocampal neurons during HIE and the potential inhibitory impact of ethyl pyruvate on this pathway. We used HE staining, immunofluorescence double staining, transmission electron microscopy, and western blot to demonstrate that EP effectively inhibited hippocampal neuronal pyroptosis and attenuated the activation of the NLRP3/Caspase‐1/GSDMD signaling pathway in HIBD rats, which resulted in a reduction of neuroinflammation and facilitated neural recovery. The results suggest that EP may be a promising neuroprotective agent for treating HIE. [ABSTRACT FROM AUTHOR]

Previous studies have shown that the ATP-P2X4 receptor signaling pathway mediates the activation of the Nod-like receptor family protein 3 (NLRP3) inflammasome. The NLRP3 inflammasome may promote renal interstitial inflammation in diabetic nephropathy. As inflammation also plays an important role in the pathogenesis of Parkinson’s disease, we hypothesized that the ATP-P2X4 receptor signaling pathway may activate the NLRP3 inflammasome in Parkinson’s disease. A male rat model of Parkinson’s disease was induced by stereotactic injection of 6-hydroxydopamine into the pars compacta of the substantia nigra. The P2X4 receptor and the NLRP3 inflammasome (interleukin-1β and interleukin-18) were activated. Intracerebroventricular injection of the selective P2X4 receptor antagonist 5-(3-bromophenyl)-1,3-dihydro-2H-benzofuro[3,2-e]-1,4-diazepin-2-one (5-BDBD) or knockdown of P2X4 receptor expression by siRNA inhibited the activation of the NLRP3 inflammasome and alleviated dopaminergic neurodegeneration and neuroinflammation. Our results suggest that the ATP-P2X4 receptor signaling pathway mediates NLRP3 inflammasome activation, dopaminergic neurodegeneration, and dopamine levels. These findings reveal a novel role of the ATP-P2X4 axis in the molecular mechanisms underlying Parkinson’s disease, thus providing a new target for treatment. This study was approved by the Animal Ethics Committee of Qingdao University, China, on March 5, 2015 (approval No. QYFYWZLL 26119).

Adsorption using biochar is a high-efficient method for removing dyes from wastewater, and it has become a hot research topic in recent years. Biochar produced from organic wastes through pyrolysis is a promising way to combine bioenergy recovery and dye removal. In this study, durian shell (DS) was used as a feedstock for biochar and bio-oil production under different pyrolysis temperatures (400, 500, and 600 °C) for bioenergy recovery. Then, the biochar was applied as the absorbent for methylene blue (MB) removal from wastewater under batch and continuous experiments. It was found that the bio-oil production was slightly affected by temperature, while the productivity of biochar decreased from 42.05% to 30.65% with the increase in pyrolysis temperature from 400 to 600 °C. Compared with the biochar produced at 500 °C (DS-500) and 600 °C (DS-600), the biochar obtained at 400 °C (DS-400) exhibited higher MB removal efficiency and adsorption capacity under various pH conditions due to the superior microstructure. A high pH condition was beneficial for the adsorption process with DS-400. Additionally, the MB removal efficiencies increased with the increase in biochar dosage by providing more activated sites. A high MB content can promote the adsorption process, but a too high MB content negatively affects the removal efficiency due to the sorption saturation. Adsorption processes are more likely to match a pseudo-second-order model by chemical reactions. In the long-term continuous experiment, MB can be effectively removed to match the discharge standard by DS-400. This study provided a sustainable pathway for organic waste disposal and dye wastewater treatment. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress (OS) plays a major role in the progress of hypoxic‐ischemic brain damage (HIBD). This study aimed to investigate OS‐related genes and their underlying molecular mechanisms in neonatal HIBD. Methods: Microarray data sets were acquired from the Gene Expression Omnibus (GEO) database to screen the differentially expressed genes (DEGs) between control samples and HIBD samples. OS‐related genes were drawn from GeneCards and OS‐DEGs in HIBD were obtained by intersecting with the DEGs. Subsequently, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were conducted to determine the underlying mechanisms and functions of OS‐DEGs in HIBD. Moreover, the hub genes were screened using the protein−protein interaction network and identified in the GSE144456 data set. CIBERSORT was then performed to evaluate the expression of immunocytes in each sample and perform a correlation analysis of the optimal OS‐DEGs and immunocytes. Finally, quantitative reverse transcription polymerase chain reaction (RT‐qPCR) and immunohistochemistry were performed to validate the expression levels of the optimal OS‐DEGs. Results: In total, 93 OS‐DEGs were identified. GO, KEGG, and GSEA enrichment analyses indicated that these genes were predominantly enriched in OS and inflammation. Four OS‐related biomarker genes (Jun, Fos, Tlr2, and Atf3) were identified and verified. CIBERSORT analysis revealed the dysregulation of six types of immune cells in the HIBD group. Moreover, 47 drugs that might target four OS‐related biomarker genes were screened. Eventually, RT‐qPCR and immunohistochemistry results for rat samples further validated the expression levels of Fos, Tlr2, and Atf3. Conclusions: Fos, Tlr2 and Atf3 are potential OS‐related biomarkers of HIBD progression. The mechanisms of OS are associated with those of neonatal HIBD. [ABSTRACT FROM AUTHOR]

Polymeric materials, rich in carbon, hydrogen, and oxygen elements, present substantial fire hazards to both human life and property due to their intrinsic flammability. Overcoming this challenge in the absence of any flame-retardant elements is a daunting task. Herein, we introduce an innovative strategy employing catalytic polymer auto-pyrolysis before combustion to proactively release CO2, akin to possessing responsive CO2 fire extinguishing mechanisms. We demonstrate that potassium salts with strong nucleophilicity (such as potassium formate/malate) can transform conventional polyurethane foam into materials with fire safety through rearrangement. This transformation results in the rapid generation of a substantial volume of CO2, occurring before the onset of intense decomposition, effectively extinguishing fires. The inclusion of just 1.05 wt% potassium formate can significantly raise the limiting oxygen index of polyurethane foam to 26.5%, increase the time to ignition by 927%, and tremendously reduce smoke toxicity by 95%. The successful application of various potassium salts, combined with a comprehensive examination of the underlying mechanisms, underscores the viability of this strategy. This pioneering catalytic approach paves the way for the efficient and eco-friendly development of polymeric materials with fire safety. Overcoming this challenge of fire hazards by carbon, hydrogen, and oxygen rich materials remains challenging. Here, the authors demonstarte that catalytic polymer auto-pyrolysis before combustion releases CO2, equipping the material with fire retardant properties. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress is one of the key contributors to cellular senescence and ovarian aging. Quercetin has a variety of physiological activities such as antioxidant. Given that hydrogen peroxide can cause oxidative damage to cells, the present study is designed to verify the protective effect of quercetin on human ovarian granulosa tumor cell line under oxidative stress. Methods: Cell counting kit-8 and lactate dehydrogenase assays examined cell viability and toxicity. Flow cytometry detected reactive oxygen species accumulation. Glutathione level was measured to analyze the oxidation resistance. Cell apoptosis was evaluated by Hoechst 33258 staining, acridine orange/Ethidium Bromide staining and western blot. The mitochondrial structure was observed under a transmission electron microscope. Mitochondrial membrane integrity was detected by JC-1 staining and western blot. Results: Hydrogen peroxide could induce cell injury, promote reactive oxygen species accumulation, and lead to glutathione depletion. hydrogen peroxide also resulted in mitochondrial morphological damage and depolarization, which activate caspase3/9 subsequently. However, quercetin could mitigate these damages. Conclusions: Present study found that hydrogen peroxide induced oxidative stress and mitochondrial apoptosis of human ovarian granulosa tumor cell line cells, which could be attenuated by quercetin. [ABSTRACT FROM AUTHOR]

Abstract Background Jiangtang decoction (JTD) is a China patented drug which contains Euphorbia humifusa Willd, Salvia miltiorrhiza Bunge, Astragalus mongholicus Bunge, Anemarrhena asphodeloides Bunge, and Coptis chinensis Franch. For decades, it has also been used clinically to treat diabetic nephropathy (DN) effectively; however, the associated mechanisms remain unknown. Thus, the present study aimed to examine the protective efficacy of JTD in DN and elucidate the underlying molecular mechanisms. Methods A diabetic model using KK-Ay mice received a daily administration of JTD for 12 weeks. Body weight, blood glucose, triglycerides (TGs), total cholesterol (TC), urea nitrogen (UN), creatinine (Cr), and microalbumin/urine creatinine (MA/UCREA) was measured every 4 weeks. Furthermore, on the day of the sacrifice, blood, urine, and kidneys were collected to assess renal function according to general parameters. Pathological staining was performed to evaluate the protective renal effect of JTD. In addition, the levels of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin [IL]-6 and intercellular adhesion molecule [ICAM]-1), insulin receptor substrate [IRS]-1, advanced glycation end products [AGEs], and receptor of glycation end products [RAGE] were assessed. Finally, the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway and involvement of nuclear factor-κB (NF-κB) was further analyzed. Results After 12 weeks of metformin and JTD administration, the mice exhibited a significant amelioration in glucose and lipid metabolism dysfunction, reduced morphological changes in the renal tissue, decreased urinary albumin excretion, and normalized creatinine clearance. JTD treatment also reduced the accumulation of AGEs and RAGE, up-regulated IRS-1, and increased the phosphorylation of both PI3K (p85) and Akt, indicating that the activation of the PI3K/Akt signaling pathway was involved. Additionally, JTD administration reduced the elevated levels of renal inflammatory mediators and decreased the phosphorylation of NF-κB p65. Conclusions These results demonstrate that JTD might reduce inflammation in DN through the PI3K/Akt and NF-κB signaling pathways.