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Abstract Soluble vector family member 6 (SLC2A6) has been implicated in the aggressiveness and poor prognosis of various cancers, yet its specific role in hepatocellular carcinoma (HCC) remains to be fully elucidated. This study utilized multiple databases to investigate the relationship between SLC2A6 expression and clinical stage, methylation status, drug sensitivity, immune infiltration, and immune checkpoint regulation. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted. Furthermore, in vitro and in vivo experiments were performed to assess the impact of SLC2A6 knockout on the proliferation, migration, invasion, and underlying mechanisms in hepatocellular carcinoma (LIHC) cells. SLC2A6 expression was significantly correlated with tumor prognosis, clinical stage, and methylation levels, and was found to influence immune cell infiltration and immune checkpoint gene expression. In LIHC, SLC2A6 was associated with key biological processes, including the cell cycle, P53 signaling, and ferroptosis. Knockdown of SLC2A6 markedly suppressed the proliferation, migration, and invasion of HCC cells, with this inhibition being closely tied to the ferroptosis pathway. SLC2A6 plays a pivotal role in the regulation of pan-cancer processes, particularly in tumor prognosis and immune-related mechanisms. In LIHC, it emerges as a potential prognostic biomarker and therapeutic target for the regulation of ferroptosis, offering new insights for targeted cancer therapies.

ObjectNeuroinflammation mediated by microglia has emerged as a critical factor in ischemic stroke and neuronal damage. Gualou Guizhi Granule (GLGZG) has been shown to suppress inflammation in lipopolysaccharide (LPS)-activated microglia, though the underlying mechanisms and its protective effects against neuronal apoptosis remain unclear. This study aims to investigate how GLGZG regulates the Notch signaling pathway in microglia to reduce neuroinflammation and protect neurons from apoptosis.MethodUsing in vitro and in vivo models, we explored GLGZG's impact on microglia activation, pro-inflammatory cytokines, and neuronal apoptosis. Microglial cells were activated with LPS, and primary neuronal cells were exposed to LPS-activated microglia to simulate neuroinflammation. Additionally, we investigated the effects of GLGZG in combination with N-[N-[3,5-difluorophenacetyl]-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) or siRNA-Notch1 to further elucidate the involvement of the Notch signaling pathway.ResultsGLGZG significantly inhibited microglia activation and reduced neuroinflammation by de-creasing the levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in both in vitro and in vivo models. GLGZG also effectively protected against microglia-induced neuronal apoptosis. Mechanistically, GLGZG down-regulated key components of the Notch signaling pathway, in-cluding Notch-1, NICD, RBPSUH, and Hes-1, in activated microglia. Combined treatment with GLGZG and DAPT or siRNA-Notch1 demonstrated enhanced inhibition of microglial activation and neuroinflammation.ConclusionOur findings reveal that GLGZG exerts its protective effects through the suppression of the Notch signaling pathway, thereby inhibiting microglia activation, reducing neuroinflammation, and safeguarding neurons from neuroinflammation-induced damage, offering potential as a therapeutic agent for ischemic stroke-induced neuroinflammation.

Background1-Bromoacetyl-3,3-dinitroazetidine (RRx-001) has potent antitumor effects, indicating its promising therapeutic potential against various cancers. This research investigates RRx-001 activity against hepatocellular carcinoma (HCC) and elucidates its underlying mechanisms.MethodsHuh7, Hepa1-6, and MHCC97H cells were cultured and treated with varying RRx-001 concentrations for 24, 48, and 72 h. Cell viability was assessed using cell counting kit-8. The cells were divided into control and RRx-001 treatment groups at 0.5 × IC50, 1.0 × IC50, and 2.0 × IC50 concentrations for each cell line. Migration and invasion were evaluated using scratch and Transwell assays, and apoptosis was examined by apoptosis assays. RNA sequencing was performed on the Huh7 cells treated with RRx-001 for 24 h to identify differential gene expression. CD47 and TP53 protein levels were measured by Western blot. A xenograft mouse model was utilized to evaluate the effect of RRx-001 on HCC.ResultsRRx-001 inhibits HCC cell viability, migration, and invasion while inducing apoptosis, These effects are potentially mediated by the downregulation of CD47 and the upregulation of TP53, both of which modulate key signaling pathways. In vivo experiments demonstrated that RRx-001 effectively inhibits tumor growth.ConclusionRRx-001 reduces the viability of HCC cells and induces apoptosis. This effect may be due to the downregulation of CD47 expression and the alteration of the TP53 protein regulatory pathway.

The Double U-pipe ground heat exchanger, known for its simple process, cost-effectiveness, high heat exchange efficiency, and low thermal resistance, remains the predominant type of ground heat exchanger in today’s shallow geothermal energy development and utilization. In recent years, significant research has focused on the factors influencing heat transfer and the heat exchange performance of Double U-pipe ground heat exchangers through experimental testing methods. However, studies that integrate numerical simulation with in situ testing have been less common. Utilizing the cylindrical heat source model theory and the results of regional in situ thermal response tests, this paper develops a Double U-pipe ground heat transfer model by establishing physical, mathematical, and heat transfer geometric models. It evaluates the effects of varying inlet temperatures, flow rates, and initial ground temperatures on heat exchange efficiency under heating conditions. The results confirm the accuracy of the Double U-pipe ground heat exchanger model based on in situ testing. They indicate that increasing the temperature differential between the inlet and initial temperatures, raising the initial ground temperature, and moderately enhancing the flow rate can improve the system’s heat exchange efficiency.

Ethnopharmacological relevance: Pien-Tze-Huang (PZH)—a traditional Chinese medicine (TCM) compound—has been employed to treat various liver inflammation and tumors for over 10 decades. Interestingly, most of the pharmacological effects had been validated and explored toward liver ailment along with pro-inflammatory conditions and cancer at the cellular and molecular level to date.Aim of the study: The present study aimed to investigate the therapeutic effect of PZH on autophagy and TGF-β1 signaling pathways in rats with liver fibrosis and hepatic stellate cell line (HSC).Materials and methods: Male SD rats with carbon tetrachloride (CCl4)-induced liver fibrosis were used as the animal model. Next, PZH treatment was given for 8 weeks. Afterward, the therapeutic effects of PZH were analyzed through a hepatic tissue structure by hematoxylin-eosin (H&E), Van Gieson (VG) staining, and transmission electron microscopy (TEM), activity of ALT and AST by enzyme-associated immunosorbent assay as well. Subsequently, mRNA and protein expression were examined by quantitative polymerase chain reaction (qPCR), Western blotting, and immunohistochemistry (IHC). Then, the cell vitality of PZH-treated HSC and the expression of key molecules prevailing to autophagy were studied in vitro. Meanwhile, SM16 (a novel small molecular inhibitor which inhibits TGFβ-induced Smad2 phosphorylation) was employed to confirm PZH’s effects on the proliferation and autophagy of HSC.Results: PZH pharmacologically exerted anti-hepatic fibrosis effects as demonstrated by protecting hepatocytes and improving hepatic function. The results revealed the reduced production of extracellular collagen by adjusting the balance of matrix metalloproteinase (MMP) 2, MMP9, and tissue inhibitor of matrix metalloproteinase 1 (TIMP1) in PZH-treated CCl4-induced liver fibrosis. Interestingly, PZH inhibited the activation of HSC by down-regulating TGF-β1 and phosphorylating Smad2. Furthermore, PZH down-regulated yeast Atg6 (Beclin-1) and microtubule-associated protein light chain 3 (LC3) toward suppressing HSC autophagy, and PZH exhibited similar effects to that of SM16.Conclusion: To conclude, PZH alleviated CCl4-induced liver fibrosis to reduce the production of extracellular collagen and inhibiting the activation of HSC. In addition, their pharmacological mechanisms related to autophagy and TGF-β1/Smad2 signaling pathways were revealed for the first time.

Ethnopharmacological relevance: Pien-Tze-Huang (PZH)--a traditional Chinese medicine (TCM) compound--has been employed to treat various liver inflammation and tumors for over 10 decades. Interestingly, most of the pharmacological effects had been validated and explored toward liver ailment along with pro-inflammatory conditions and cancer at the cellular and molecular level to date. Aim of the study: The present study aimed to investigate the therapeutic effect of PZH on autophagy and TGF-β1 signaling pathways in rats with liver fibrosis and hepatic stellate cell line (HSC). Materials and methods: Male SD rats with carbon tetrachloride (CCl4)-induced liver fibrosis were used as the animal model. Next, PZH treatment was given for 8 weeks. Afterward, the therapeutic effects of PZH were analyzed through a hepatic tissue structure by hematoxylin-eosin (H&E), Van Gieson (VG) staining, and transmission electron microscopy (TEM), activity of ALT and AST by enzyme-associated immunosorbent assay as well. Subsequently, mRNA and protein expression were examined by quantitative polymerase chain reaction (qPCR), Western blotting, and immunohistochemistry (IHC). Then, the cell vitality of PZH-treated HSC and the expression of key molecules prevailing to autophagy were studied in vitro. Meanwhile, SM16 (a novel small molecular inhibitor which inhibits TGFβ-induced Smad2 phosphorylation) was employed to confirm PZH's effects on the proliferation and autophagy of HSC. Results: PZH pharmacologically exerted anti-hepatic fibrosis effects as demonstrated by protecting hepatocytes and improving hepatic function. The results revealed the reduced production of extracellular collagen by adjusting the balance of matrix metalloproteinase (MMP) 2, MMP9, and tissue inhibitor of matrix metalloproteinase 1 (TIMP1) in PZH-treated CCl4-induced liver fibrosis. Interestingly, PZH inhibited the activation of HSC by down-regulating TGF-β1 and phosphorylating Smad2. Furthermore, PZH down-regulated yeast Atg6 (Beclin-1) and microtubule-associated protein light chain 3 (LC3) toward suppressing HSC autophagy, and PZH exhibited similar effects to that of SM16. Conclusion: To conclude, PZH alleviated CCl4-induced liver fibrosis to reduce the production of extracellular collagen and inhibiting the activation of HSC. In addition, their pharmacological mechanisms related to autophagy and TGF-β1/Smad2 signaling pathways were revealed for the first time. [ABSTRACT FROM AUTHOR]

We present measurements of the 2p-3d transition opacity of a hot molybdenum–scandium sample with nearly half-vacant molybdenum M-shell configurations. A plastic-tamped molybdenum–scandium foil sample is radiatively heated to high temperature in a compact D-shaped gold Hohlraum driven by ∼30 kJ laser energy at the SG-100 kJ laser facility. X rays transmitted through the molybdenum and scandium plasmas are diffracted by crystals and finally recorded by image plates. The electron temperatures in the sample in particular spatial and temporal zones are determined by the K-shell absorption of the scandium plasma. A combination of the IRAD3D view factor code and the MULTI hydrodynamic code is used to simulate the spatial distribution and temporal behavior of the sample temperature and density. The inferred temperature in the molybdenum plasma reaches a average of 138 ± 11 eV. A detailed configuration-accounting calculation of the n = 2–3 transition absorption of the molybdenum plasma is compared with experimental measurements and quite good agreement is found. The present measurements provide an opportunity to test opacity models for complicated M-shell configurations.

IntroductionContinuous cropping obstacle seriously affects the quality and yield of Salvia miltiorrhiza, and the synergistic effect of root exudates and rhizosphere pathogenic microorganisms may be an important cause of continuous cropping obstacle. This study aimed to explore the effects of representative organic acids on the growth and metabolism of specific microorganisms in the S. miltiorrhiza rhizosphere soil under continuous cropping, and clarify its mechanism.MethodsThe effect of phthalic acid (PA) on the growth and metabolism of Rhizoctonia solani was evaluated by mycelial growth inhibition method. Ultra-high performance liquid chromatography and tandem mass spectrometry were used to identify the differential metabolites of R. solani induced by exogenous PA.ResultsPA exerted a concentration-dependent effect on mycelial growth, biomass, intracellular polysaccharides con-tent, and total protein content in R. solani. A total of 1773 metabolites and 1040 differential metabolites were identified in the blank medium (CK), Fungi (CK + fungi), and PA-Fungi (CK + fungi + acid) groups. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis showed that the differential metabolites were mainly involved in the sugar, lipid, and protein metabolic pathways related to stable membrane structure and cell growth.DiscussionThe proliferation and metabolism network of R. solani induced by PA was proposed, and the enhancement of sugar, lipid, and amino acid metabolism was presumed to be related to the active resistance of cells to organic acid stress. These results offer new in-sights into the effects of PA metabolism on promoting R. solani proliferation, and provide theoretical support for further optimizing the rhizosphere microecological environment of Salvia miltiorrhiza continuous cropping soil and reducing continuous cropping obstacle.

Sweet potato (Ipomoea batatas (L.) Lam.) is one of the most widely cultivated crops in the world, with outstanding stress tolerance, but drought stress can lead to a significant decrease in its yield. To reveal the response mechanism of sweet potato to drought stress, an integrated physiological, transcriptome and metabolome investigations were conducted in the leaves of two sweet potato varieties, drought-tolerant zhenghong23 (Z23) and a more sensitive variety, jinong432 (J432). The results for the physiological indexes of drought showed that the peroxidase (POD) and superoxide dismutase (SOD) activities of Z23 were 3.68 and 1.21 times higher than those of J432 under severe drought, while Z23 had a higher antioxidant capacity. Transcriptome and metabolome analysis showed the importance of the amino acid metabolism, respiratory metabolism, and antioxidant systems in drought tolerance. In Z23, amino acids such as asparagine participated in energy production during drought by providing substrates for the citrate cycle (TCA cycle) and glycolysis (EMP). A stronger respiratory metabolism ability could better maintain the energy supply level under drought stress. Drought stress also activated the expression of the genes encoding to antioxidant enzymes and the biosynthesis of flavonoids such as rutin, resulting in improved tolerance to drought. This study provides new insights into the molecular mechanisms of drought tolerance in sweet potato.

Experiments and simulations have been carried out to study the colliding process by two lasers irradiating a gold half-hohlraum. Via analyzing the evolutionary x-ray images, radiation fluxes and self-emission spectrum of tracers, influence on the x-ray conversion efficiency and the local plasma temperature $T_{e,i}$ from two gold-plasma plumes have been investigated deeply, which is similar as the configuration in Inertial Confinement Fusion (ICF). Experimental results confirm a region with high electron and ion temperatures $T_{e,i}$ are induced, satisfying the strong collision condition of $\lambda_{i} \lt \Delta{L}$ , where λ _i and $\Delta{L}$ are respectively the ion mean-free path and the gradient length of T _e . It leads to almost $30\%$ increasing of M-band component compared to that from a single laser-irradiation case. Meanwhile ion temperature in this region increases more rapidly than electrons, reaching about $T_i\approx(16\pm4)$ keV ( $T_e\approx(2\pm 0.2)$ keV). Thus, our studies provide the experimental evidence of quantitative x-ray enhancement and a non-equilibrium evolution simultaneously due to the plasma collision for the first time. Besides, two-dimensional simulation results reveal that this process can not be precisely described by the traditional shock-heating model by dissipating the shock energy only to ions. But by distributing the viscous heating between both electrons and ions as theoretically discussed by Miller (2020 Comput. Fluids 210 104672), numerical results can match experiments better. This discovery will be of great importance to improve the precision of prediction for ICF.

Abstract Background Cell pyroptosis has been characterized by cell swelling and pro-inflammatory factors release to aggravate inflammatory reaction., such as interlukin-1 beta (IL-1β) and interlukin18 (IL-18). However, the function of famotidine, an antagonist of histamine H2-receptor antagonists, in cell pyroptosis remained unknown. Methods Real-time quantitative PCR (qPCR), western blotting (WB), LDH release assay and enzyme linked immunosorbent assay (Elisa) combined with inhibitor were performed to analyze the effect of famotidine on cell pyroptosis-related gene expression. Results In this study, we found that famotidine (300 μm) treatment led to a phenomenon of cell pyroptosis as confirmed by LDH assay. Further results showed that famotidine triggered cell pyroptosis in gastric cancer cells by activation of NLPR3 inflammasomes including ASC, Caspase-1 and NLRP, leading to enhanced IL-18, not IL-1β, mature and secretion. What’s more, the results also showed GSDME, not GSDMD, was increased in response to famotidine stimulation in BGC823 and AGS cells. Mechanically, phosphorylation of ERK1/2 was drastically enhanced in present with famotidine treatment, while inhibition of ERK1/2 activity by U0126 could reverse the promotion of famotidine in IL-18 secretion. Conclusion These findings revealed a novel role of famotidine in cell pyroptosis in patients with gastric cancer, a comprehensive consideration is needed in treatment of gastric cancer.

Objective(s): The aims of the present study were to investigate the expression of calcium sensing receptor (CaSR) at different times in acute myocardial infarction (AMI) rat myocardial tissue after mouse embryonic stem cells (mESCs) transplantation treatment and to assess its effects on apoptosis and oxidative stress of cardiomyocytes. Materials and Methods: The AMI rats were treated with mESCs, Calindol (a CaSR agonist) and Calhex231 (a CaSR inhibitor). Serum measurements, Echocardiographic analysis and TUNEL assay were performed. Myocardial ultrastructure changes were viewed by electron microscopy. Additionally, western blotting was used to detect the protein expressions.Results: Compared to the sham group, it was found that the expression levels of CaSR, caspase-3, cytoplasmic cytochrome C (cyt-C) and Bcl2-associated x (Bax), and the levels of Malondialdehyde (MDA) were significantly increased in both AMI and AMI + mESCs + Calindol groups with the development of myocardial infarction. Furthermore, the ultra-microstructure of cardiomyocyte was highly damaged, the expression levels of mitochondrial cyt-C and B-cell lymphoma 2 (Bcl-2) were significantly decreased, and there was decreased activity of superoxide dismutase (SOD). However, the combination of Calhex231 and mESCs transplantation could inhibit these changes. Conclusion: Our results suggested that CaSR expression in myocardial tissue of AMI rats was increased over time, and that Calhex231 could enhance the efficacy of ESCs transplantation for the treatment of AMI, which would be a new therapeutic strategy for the treatment of AMI.

Stem nematode disease can seriously reduce the yield of sweet potato (Ipomoea batatas (L.) Lam). To explore resistance mechanism to stem nematode in sweet potato, transcriptomes and metabolomes were sequenced and compared between two sweet potato cultivars, the resistant Zhenghong 22 and susceptible Longshu 9, at different times after stem nematode infection. In the transcriptional regulatory pathway, mitogen-activated protein kinase signaling was initiated in Zhenghong 22 at the early stage of infection to activate genes related to ethylene production. Stem nematode infection in Zhenghong 22 also triggered fatty acid metabolism and the activity of respiratory burst oxidase in the metabolic pathway, which further stimulated the glycolytic and shikimic pathways to provide raw materials for secondary metabolite biosynthesis. An integrated analysis of the secondary metabolic regulation pathway in the resistant cultivar Zhenghong 22 revealed the accumulation of tryptophan, phenylalanine, and tyrosine, leading to increased biosynthesis of phenylpropanoids and salicylic acid and enhanced activity of the alkaloid pathway. Stem nematode infection also activated the biosynthesis of terpenoids, abscisic acid, zeatin, indole, and brassinosteroid, resulting in improved resistance to stem nematode. Finally, analyses of the resistance regulation pathway and a weighted gene co-expression network analysis highlighted the importance of the genes itf14g17940 and itf12g18840, encoding a leucine-rich receptor-like protein and 1-aminocyclopropane-1-carboxylate synthase, respectively. These are candidate target genes for increasing the strength of the defense response. These results provide new ideas and a theoretical basis for understanding the mechanism of resistance to stem nematode in sweet potato.

In 2006, the indica photoperiod- and thermo-sensitive genie male sterile (PTGMS) line Yan 161S was successfully bred by crossing the Guangzhan 63S (♀) and the medium indica breeding material Yan 229 (♂), which was bred by the Institute of Agricultural Sciences in Coastal Region of Jiangsu Province, after years' and generations' selection in different areas. It passed the identification by Jiangsu Provincial Crop Variety Appraisal Committee in 2013. Crossing the Yan 161S with Yanhui 888, a new high-yielding and high-quality two-line hybrid rice combination Yanliangyou 1618 was developed, and it passed the variety identification in 2014. This paper introduced the breeding processes and characteristics of Yan 161S and Yanliangyou 1618 and the cultivation and seed production techniques of Yanliangyou 1618. [ABSTRACT FROM AUTHOR]

A 100 kJ-level laser facility has been designed to study inertial confinement fusion physics in China. This facility incorporates various diagnostic techniques, including optical, x-ray imaging, x-ray spectrum, and fusion product diagnostics, as well as general diagnostics assistance systems and central control and data acquisition systems. This paper describes recent developments in diagnostics at the facility.

Previously, we obtained the sweetpotato somatic hybrid KT1 from a cross between sweetpotato (Ipomoea batatas (L.) Lam.) cv. Kokei No. 14 and its drought-tolerant wild relative I. triloba L. KT1 not only inherited the thick storage root characteristic of Kokei No. 14 but also the drought-tolerance trait of I. triloba L. The aim of this study was to explore the molecular mechanism of the drought tolerance of KT1. Four-week-old in vitro-grown plants of KT1, Kokei No. 14, and I. triloba L. were subjected to a simulated drought stress treatment (30% PEG6000) for 0, 6, 12 and 24 h. Total RNA was extracted from samples at each time point, and then used for transcriptome sequencing. The gene transcript profiles of KT1 and its parents were compared to identify differentially expressed genes, and drought-related modules were screened by a weighted gene co-expression network analysis. The functions of ABI-like protein and Ca2+-ATPase, two proteins screened from the cyan and light yellow modules, were analyzed in terms of their potential roles in drought tolerance in KT1 and its parents. These analyses of the drought responses of KT1 and its somatic donors at the transcriptional level provide new annotations for the molecular mechanism of drought tolerance in the somatic hybrid KT1 and its parents.