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Background: The aim of the study is to evaluate clinical outcomes of patients with ovarian metastases from colorectal cancer (OM-CRC) treated with complete resection combined with chemotherapy and ...

As nitric oxide (NO) plays significant roles in a variety of physiological processes, the capability for real-time and accurate detection of NO in live organisms is in great demand. Traditional assessments of NO rely on indirect colorimetric techniques or electrochemical sensors that often comprise rigid constituent materials and can hardly satisfy sensitivity and spatial resolution simultaneously. Here, we report a flexible and highly sensitive biosensor based on organic electrochemical transistors (OECTs) capable of continuous and wireless detection of NO in biological systems. By modifying the geometry of the active channel and the gate electrodes of OECTs, devices achieve optimum signal amplification of NO. The sensor exhibits a low response limit, a wide linear range, high sensitivity, and excellent selectivity, with a miniaturized active sensing region compared with a conventional electrochemical sensor. The device demonstrates continuous detection of the nanomolar range of NO in cultured cells for hours without significant signal drift. Real-time and wireless measurement of NO is accomplished for 8 d in the articular cavity of New Zealand White rabbits with anterior cruciate ligament (ACL) rupture injuries. The observed high level of NO is associated with the onset of osteoarthritis (OA) at the later stage. The proposed device platform could provide critical information for the early diagnosis of chronic diseases and timely medical intervention to optimize therapeutic efficacy.

The hypoxic tumor microenvironment promotes both cancer progression and drug resistance.Prolyl hydroxylases are hypoxic sensor proteins that are frequently mutated or heterozygously deleted in breast cancers; however, how prolyl hydroxylation regulates breast cancer progression and drug resistance remains poorly understood. Here, we found that hypoxia promotes cancer progression and resistance to chemotherapy drugs, specifically through prolyl hydroxylation-dependent activation of MAPK signaling. We characterized a pVHL-independent mechanism wherein the prolyl hydroxylase EglN1 catalyzed prolyl hydroxylation of the proline-rich domain of RAS-specific guanine nucleotide exchange factor SOS1, thereby preventing its binding with the growth factor receptor bound protein 2 (GRB2) to block the formation of MAPK signaling microclusters in breast cancer. Inhibition of EglN1’s prolyl hydroxylase function—which occurs in hypoxic conditions and upon accumulation of fumarate—induced cancer-specific dysregulation of MAPK signaling, which promoted both breast cancer growth and resistance to MEK inhibitors. We harnessed this insight and demonstrated a therapeutic strategy that potently inhibits breast cancer growth and drug resistance based on pharmacologically disrupting the prolyl-hydroxylation-mediated interaction between SOS1 and GRB2.

In this article, the bond performance between recycled concrete and corroded steel bars is analyzed by the nonlinear numerical simulation. The result shows that the maximum bond strength between recycled concrete and steel bar decreases with the increase in steel bar corrosion rate; when the recycled concrete strength is large, the simulated maximum bond strength is in good agreement with the experimental maximum bond strength; when the recycled concrete strength is small, the simulated maximum bond strength is in relatively poor agreement with the experimental maximum bond strength, but there is still an error within the allowable range; the slip between recycled concrete and steel bar increases with the increase in steel bar corrosion rate; when the steel bar corrosion rate exceeded 5%, the bond strength decreases more rapidly; the maximum bond strength increases with the increase in specimen sizes under the same steel bar corrosion rate; the maximum bond strength decreases with the increase in steel bar diameter under the same steel bar corrosion rate.

Colon cancer, as one of the common malignant tumors, has the highest morbidity and mortality. We investigated the clinical significance and possible mechanism of the circular RNA circHIPK2 in the progression of colorectal cancer (CRC). Quantitative analysis of mRNAs, gene microarray hybridization, immunofluorescence, luciferase reporter assay, proliferation assay, EDU staining, subcellular location analysis and Western blotting. circHIPK2 expression was upregulated in patients with CRC compared with paracancerous tissues. In contrast, patients with high circHIPK2 expression had lower overall survival rate and disease-free survival rate than those with low circHIPK2 expression. circHIPK2 expression in normal intestinal epithelial cells was lower than that in CRC cell lines. circHIPK2 promoted CRC progression. miR-485-5p reduced CRC progression. miR-485-5p, as the target of circHIPK2 in CRC model, played a role in promoting CRC progression and expediting HSP90 ubiquitination. HSP90 ubiquitination by miR-485-5p can promote cell proliferation. circHIPK2 has potential clinical significance in CRC progression, which may serve as an exceptional candidate for further therapeutic exploration.

Emotion Recognition in Conversation (ERC) plays a significant part in Human-Computer Interaction (HCI) systems since it can provide empathetic services. Multimodal ERC can mitigate the drawbacks of uni-modal approaches. Recently, Graph Neural Networks (GNNs) have been widely used in a variety of fields due to their superior performance in relation modeling. In multimodal ERC, GNNs are capable of extracting both long-distance contextual information and inter-modal interactive information. Unfortunately, since existing methods such as MMGCN directly fuse multiple modalities, redundant information may be generated and diverse information may be lost. In this work, we present a directed Graph based Cross-modal Feature Complementation (GraphCFC) module that can efficiently model contextual and interactive information. GraphCFC alleviates the problem of heterogeneity gap in multimodal fusion by utilizing multiple subspace extractors and Pair-wise Cross-modal Complementary (PairCC) strategy. We extract various types of edges from the constructed graph for encoding, thus enabling GNNs to extract crucial contextual and interactive information more accurately when performing message passing. Furthermore, we design a GNN structure called GAT-MLP, which can provide a new unified network framework for multimodal learning. The experimental results on two benchmark datasets show that our GraphCFC outperforms the state-of-the-art (SOTA) approaches., 13 pages

This paper studied the mechanical performance of aerated concrete and its bonding performance with glass fiber grille, and explores the influence of aluminum powder and aluminum powder on mechanical performance and bonding performance. The results showed that the compressive strength of aerated concrete decreased with the increase of aluminum powder content, while it first increased and then decreased with the increase of ferrosilicon alloy powder content. The failure modes of specimens were fiber fracture failure, and the fibers were not pulled out from the aerated concrete. It can provide a theoretical basis for the application of aerated concrete and glass fiber in engineering.

Conventional bioelectrical sensors and systems integrate multiple power harvesting, signal amplification and data transmission components for wireless biological signal detection. This paper reports the real-time biophysical and biochemical activities can be optically captured using a microscale light-emitting diode (micro-LED), eliminating the need for complicated sensing circuit. Such a thin-film diode based device simultaneously absorbs and emits photons, enabling wireless power harvesting and signal transmission. Additionally, owing to its strong photon-recycling effects, the micro-LED’s photoluminescence (PL) emission exhibits a superlinear dependence on the external conductance. Taking advantage of these unique mechanisms, instantaneous biophysical signals including galvanic skin response, pressure and temperature, and biochemical signals like ascorbic acid concentration, can be optically monitored, and it demonstrates that such an optoelectronic sensing technique outperforms a traditional tethered, electrically based sensing circuit, in terms of its footprint, accuracy and sensitivity. This presented optoelectronic sensing approach could establish promising routes to advanced biological sensors.

Background Gastric cancer (GC) is an aggressive malignancy with high lethality. Systematic chemotherapy is the main therapeutic strategy for advanced GC patients. The overexpression of Axl is associated with poor prognosis and regulates tumor growth and metastasis in many types of cancer. However, the role of Axl in GC progression remains elusive. Materials and methods Western blot and quantitative real-time PCR assay (RT-PCR) assays were used to detect the expression of Gas6, Axl, ZEB1 and epithelial-mesenchymal transition (EMT)-related markers in GC cells. Cell proliferation was determined by EdU cell proliferation assay and CCK-8 assay. Transwell invasion assay was performed to explore the effect of Axl and ZEB1 on cell invasion. Tumor xenografts and lung metastasis models were conducted to examine the effect of Axl on the growth and lung metastasis of GC cells. Results In our study, we found that high levels of Gas6 and Axl expression were associated with reduced overall survival (OS) in GC patients and the expression of Gas6 and Axl was upregulated in GC cell lines. Ectopic expression of Axl induced EMT and promoted GC cell invasion and proliferation. The knockdown of Axl inhibited EMT and suppressed the proliferation and invasion of GC cell. In vivo study showed that inhibition of Axl impaired tumor growth and lung metastasis of GC cells. Mechanistic investigations revealed that Axl promoted EMT, invasion, and proliferation via upregulating ZEB1 expression in GC cells. Conclusion Our results demonstrated that the Gas6/Axl/ZEB1 signaling pathway regulated EMT, invasion, and proliferation in GC cells and might represent a potential therapeutic target for GC treatment.

Background The aim of this study was to evaluate the efficacy and safety of trastuzumab, combined with the FLOT regimen, in the perioperative treatment of resectable HER-2-positive advanced gastric cancer. Methods Overall, 45 patients were divided into two groups; 29 patients in the experimental group were treated with trastuzumab combined with FLOT and 16 patients in the control group were treated with FLOT alone. The primary endpoint was objective response rate (ORR), and the secondary endpoints were disease control rate (DCR), tumor regression grade (TRG), surgical margin, side effects, and overall survival. Results In the experimental and control groups, ORR was 72.4% and 43.8% (p=0.226), DCR was 89.7% and 87.5%, R0 resection rate was 96.5% and 93.7%, total/subtotal tumor regression grade was 17.2% and 6.3%, partial tumor regression grade was 27.6% and 18.7% (p=0.468), and 2-year survival rate was 78.1% and 73.9% (p=0.932), respectively. The common side effects were agranulocytosis and vomiting. There was no significant difference between the two groups. Conclusion Trastuzumab combined with FLOT has a good curative effect and safety profile in the perioperative treatment of patients with resectable HER-2-positive advanced gastric cancer. In addition, trastuzumab + FLOT had the same result as FLOT alone, as there was no significant benefit with the addition of T in the group studied.

Recent studies suggest that tumor fusion burden (TFB) is a hallmark of immune infiltration in prostate cancer, the correlation of TFB with immune microenvironment, and genomic patterns in head and neck squamous cell carcinomas (HNSC) remain largely unclear.Gene fusion, genomic, transcriptomic, and clinical data of HNSC patients from the cancer genome atlas (TCGA) database were collected to analyze the correlation of TFB with mutation patterns, tumor immune microenvironment, and survival time in HNSC patients.Human papillomavirus (HPV) (-) patients with low TFB exhibited significantly enhanced CD8+ T cells infiltration and cytolysis activity and increased level of interferon-gamma (IL-γ), human leukocyte antigen (HLA) class I, and chemokines. Moreover, TFB was positively correlated with TP53 mutation, score of gene copy number, and loss of heterozygosity (LOH), as well as the biological progress of epithelial-mesenchymal transition (EMT), metastasis, and stem cell characteristics. Further analysis revealed that HPV (-) HNSC patients with low TFB have a better prognosis.Our data revealed the correlation of TFB with tumor immune microenvironment and predictive features for immunotherapy, implying tumors with low TFB may be potential candidates for immunotherapeutic agents. Moreover, the TFB low group had prolonged overall survival (OS) in the HPV (-) HNSC cohort.

Defect engineering is capable of significantly enhancing catalytic performance of target materials, but very few high efficiency defect-engineered catalysts were reported due to the lacking of systematic and comprehensive understanding of defect effect, as well as controllable experimental practice. Here, we reported high-efficiency oxygen reduction reaction (ORR) nanocarbon shell electrocatalyst, using a unique localized micro-deflagration strategy combined with postprocessing of heat treatment. This micro-deflagration allows the ultrafast and large scale formation of highly porous nanocarbon structure with rich nitrogen doping, where parts of nitrogen can be further removed via post heat treatment for constituting targeted active sites of defects for ORR. The defective nanocarbon shells demonstrate large specific surface area (540 m2g-1) with 6.05 at% N-doping, which allows exceptional electrocatalytic activity (Eonset of 0.89 V vs.RHE, E1/2 of 0.79 V vs.RHE and Jk of 5.26 mA cm−2), long-term stability, and tolerance to crossover effect, comparable to commercial Pt/C in alkaline electrolyte. Most importantly, this localized micro-deflagration is significantly enriched the research of defect engineering chemical electrocatalyst, and great promising for the synthesis of other metal-free nanocarbon materials.

A high-fat diet (HFD) is reported to exacerbate ulcerative colitis by inducing obesity, which conceals the effect of the diet itself. Ferroptosis, a type of regulated cell death induced by lipid hydroperoxides, has recently been reported in colitis. Here, we aimed to determine whether HFD affects ferroptosis and colitis progression in an obesity-independent manner. We subjected male C57BL/6J mice to either an HFD (60% fat diet) or isocaloric control diet (10% fat diet) for 4 weeks, followed by inducing colitis with 2.5% dextran sulfate sodium (DSS). Compared with the isocaloric control diet, non-obesogenic HFD reduced DSS-induced colonic mucosal injury, as shown by disease activity index, colon thickness, inflammatory infiltrations, and mucosal damage index; however, there were no differences in body weight, Lee's index, and omental fat weight between the two groups. HFD mice exhibited decreased lipid peroxidation and ferroptosis markers expression in colon tissues. Furthermore, a lipid mixture protected gut organoids and normal colonic epithelial cells from RSL3-induced ferroptosis. Mechanistically, the lipid mixture prevented glutathione deficiency by upregulating the cysteine transporter, solute carrier family seven member 11. Collectively, these findings suggest that an HFD ameliorates DSS-induced colitis through ferroptosis repression in an obesity-independent manner and provide new evidence to evaluate the effects of an HFD on colitis.

Endoplasmic reticulum (ER) stress is a significant mechanism for chemoresistance to colorectal cancer (CRC) treatment. The RNA-like endoplasmic reticulum kinase (PERK) is critical for ER stress induction. In the present study, we attempted to explore whether PERK activator CCT020312 (CCT) could be effective for CRC treatment, and reveal the underlying mechanisms. We first found that CCT dose- and time-dependently reduced CRC cell proliferation. Importantly, it markedly improved the chemosensitivity of CRC cells that were drug-sensitive or -resistant to taxol treatment, as evidenced by the significantly decreased cell viability. Moreover, CCT at the non-toxic concentration exhibited obviously synergistic effects with taxol to induce apoptosis and cell cycle arrest in G2/M phase in vitro. In addition, we showed that CCT alone considerably induced ER stress in CRC cells through a dose- and time-dependent fashion. Meanwhile, CCT combined with taxol caused significant ER stress through improving phosphorylated PERK, eukaryotic translation initiation factor 2α (eIF2ɑ), C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78). More studies showed that the interaction between PERK and GRP78 was a potential target for CCT to perform its regulatory events. Intriguingly, PERK knockdown markedly abolished the regulatory role of CCT and taxol cotreatments in cell proliferation suppression and apoptosis induction, indicating the importance of PERK for CCT to perform its anti-cancer bioactivity. Our in vivo experiments confirmed that CCT plus taxol dramatically reduced tumor growth in CRC xenografts. Together, all these results suggested that promoting PERK activation by CCT may be an effective therapeutic strategy to improve CRC to taxol treatment.

Conventional epidermal electronics integrate multiple power harvesting, signal amplification and data transmission components for wireless biophysical and biochemical signal detection. This paper reports the real-time electrodermal activities can be optically captured using a microscale light-emitting diode (micro-LED), eliminating the need for complicated sensing circuit. Owing to its strong photon-recycling effects, the micro-LED’s photoluminescence (PL) emission exhibits a superlinear dependence on the external resistance. Taking advantage of this unique mechanism, the galvanic skin response (GSR) of a human subject is optically monitored, and it demonstrates that such an optoelectronic sensing technique outperforms a traditional tethered, electrically based GSR sensing circuit, in terms of its footprint, accuracy and sensitivity. This presented optoelectronic sensing approach could establish promising routes to advanced biological sensors.

Photon upconversion with the transformation of low-energy photons to high-energy photons is of significant interest for broad applications. Here, we present self-powered, micrometer-scale optoelectronic devices based on III-V materials for high-performance near-infrared to visible upconversion. By taking advantage of its unique photon – “free electron” – photon processes, these thin-film, ultra-miniaturized devices realize fast upconversion that is linearly dependent on incoherent, low-power excitation, with a quantum yield of ~1.5%. By exploiting the advanced manufacturing method, encapsulated, freestanding devices are transferred onto heterogeneous substrates and show desirable biocompatibilities within biological fluids and tissues. These devices as the microscale light sources are implanted in behaving animals, with in vitro and in vivo experiments demonstrating their utility for optogenetic neuromodulation. These results provide routes for high-performance upconversion materials and devices and their unprecedented potential as optical biointerfaces.

Background Gastric cancer (GC) is an aggressive malignancy with high lethality. Systematic chemotherapy is the main therapeutic strategy for advanced GC patients. The overexpression of Axl is associated with poor prognosis and regulates tumor growth and metastasis in many types of cancer. However, the role of Axl in GC progression remains elusive. Materials and Methods Western blot and quantitative real-time PCR assay (RT-PCR) assays were used to detect the expression of Gas6, Axl, ZEB1 and epithelial-mesenchymal transition (EMT)-related markers in GC cells. Cell proliferation was determined by EdU cell proliferation assay and CCK-8 assay. Transwell invasion assay was performed to explore the effect of Axl and ZEB1 on cell invasion. Tumor xenografts and lung metastasis models were conducted to examine the effect of Axl on the growth and lung metastasis of GC cells. Results In our study, we found that high levels of Gas6 and Axl expression were associated with reduced overall survival (OS) in GC patients and the expression of Gas6 and Axl was upregulated in GC cell lines. Ectopic expression of Axl induced EMT and promoted GC cell invasion and proliferation. The knockdown of Axl inhibited EMT and suppressed the proliferation and invasion of GC cell. In vivo study showed that inhibition of Axl impaired tumor growth and lung metastasis of GC cells. Mechanistic investigations revealed that Axl promoted EMT, invasion, and proliferation via upregulating ZEB1 expression in GC cells. Conclusion Our results demonstrated that the Gas6/Axl/ZEB1 signaling pathway regulated EMT, invasion, and proliferation in GC cells and might represent a potential therapeutic target for GC treatment.

Photon upconversion with the transformation of low-energy photons to high-energy photons is of significant interest for broad applications in biomedicine for stimulation, sensing, and imaging. Conventional upconversion materials rely on non-linear light-matter interactions, exhibit incidence dependent efficiencies and require high power excitation. Here, we present self-powered, micrometer-scale optoelectronic devices for high-performance near-infrared (~810 nm) to visible (630 nm red or 590 nm yellow) photon upconversion. Thanks to its unique photon–electron conversion process, these thin-film, ultra-miniaturized devices realize fast upconversion that is linearly dependent on incoherent, low-power excitation, with a quantum yield of ~1.5%. Encapsulated, freestanding devices are transferred onto heterogeneous flexible substrates and show desirable biocompatibilities within biological fluids and tissues. Demonstrations of optogenetic stimulation with upconversion devices as implantable light sources have successfully performed in vitro and in vivo scenarios. This approach provides a versatile route to achieve upconversion throughout the entire visible spectral range at lower power and higher efficiency than has previously been possible.

A facile calcination method is developed for the in situ synthesis of nanohybrids of Ti3+ self-doped TiO2 /graphene quantum dot nanosheets (Ti3+ -TiO2 /GQD NSs). Ti3+ sites are formed on the surface of the TiO2 nanosheets through carbothermal reduction by GQDs, using citric acid as a carbon source. Such heterojunctions exhibit enhanced visible-light absorption properties, large photocurrent current densities, and low recombination of photoinduced carriers. The methylene blue (MB) and rhodamine B (RhB) photodegradation result demonstrates a higher visible-light photocatalysis performance than that of the original TiO2 . On one hand, inducing Ti3+ sites is efficient for the separation of photogenerated charge carriers and for reducing electron-hole pair recombination. On the other hand, GQDs are beneficial for generating more photocurrent carriers and facilitating the charge transfer across the TiO2 surface. It is proposed that Ti3+ sites and GQDs induced in TiO2 nanosheets have a synergistic effect, leading to excellent photocatalysis properties. Finally, a theoretical calculation is provided of the carbothermal reduction for the formation mechanism of the Ti3+ defect sites.

Background Alpha lipoic acid (α -LA) is a naturally occurring antioxidant and metabolic enzyme co-factor. Recently, α -LA has been reported to inhibit the growth of various cancer cells, but the precise signaling pathways that mediate the effects of α -LA on non-small cell lung cancer (NSCLC) development remain unclear. Methods The CCK-8 assay was used to assess cell proliferation in NSCLC cell lines after α -LA treatment. The expression of growth factor receptor-bound protein 2 (Grb2), cyclin-dependent kinase (CDK)-2, CDK4, CDK6, Cyclin D3, Cyclin E1, Ras, c-Raf, epidermal growth factor receptor (EGFR), ERK1/2 and activated EGFR and ERK1/2 was evaluated by western blotting. Grb2 levels were restored in α-LA-treated cells by transfection of a plasmid carrying Grb2 and were reduced in NSCLC cells via specific siRNA-mediated knockdown. Results α -LA dramatically decreased NSCLC cell proliferation by downregulating Grb2; in contrast, Grb2 overexpression significantly prevented α-LA-induced decrease in cell growth in vitro. Western blot analysis indicated that α-LA decreased the levels of phospho-EGFR, CDK2/4/6, Cyclins D3 and E1, which are associated with the inhibition of G1/S-phase transition. Additional experiments indicated that Grb2 inhibition partially abolished EGF-induced phospho-EGFR and phospho-ERK1/2 activity. In addition, α-LA exerted greater inhibitory effects than gefitinib on NSCLC cells by preventing EGF-induced EGFR activation. Conclusion For the first time, these findings provide the first evidence that α-LA inhibits cell proliferation through Grb2 by suppressing EGFR phosphorylation and that MAPK/ERK is involved in this pathway.

We performed the multi-omic characterization of gastric cancer to detect key molecular features for neoadjuvant chemotherapy., Neoadjuvant chemotherapy is a common treatment for patients with gastric cancer. Although its benefits have been demonstrated, neoadjuvant chemotherapy is underutilized in gastric cancer management, because of the lack of biomarkers for patient selection and a limited understanding of resistance mechanisms. Here, we performed whole-genome, whole-exome, and RNA sequencing on 84 clinical samples (including matched pre- and posttreatment tumors) from 35 patients whose responses to neoadjuvant chemotherapy were rigorously defined. We observed increased microsatellite instability and mutation burden in nonresponse tumors. Through comparisons of response versus nonresponse tumors and pre- versus posttreatment samples, we found that C10orf71 mutations were associated with treatment resistance, which was supported by drug response data and potentially through inhibition of cell cycle, and that MYC amplification correlated with treatment sensitivity, whereas MDM2 amplification showed the opposite pattern. Neoadjuvant chemotherapy also reshapes tumor-immune signaling and microenvironment. Our study provides a critical basis for developing precision neoadjuvant regimens.

Physical and chemical technologies have been continuously progressing advances of neuroscience research. The development of research tools for closed-loop control and monitoring neural activities in behaving animals is highly desirable. In this paper, we introduce a wirelessly operated, miniaturized microprobe system for optical interrogation and neurochemical sensing in the deep brain. Via epitaxial liftoff and transfer printing, microscale light emitting diodes (micro-LEDs) as light sources, and poly(3,4-ethylenedioxythiophene) polystyrene sulfonate (PEDOT:PSS) coated diamond films as electrochemical sensors are vertically assembled to form implantable optoelectrochemical probes, for real-time optogenetic stimulation and dopamine detection capabilities. A customized, lightweight circuit module is employed for untethered, remote signal control and data acquisition. Injected into the ventral tegmental area (VTA) of freely behaving mice, in vivo experiments clearly demonstrate the utilities of the multifunctional optoelectrochemical microprobe system for optogenetic interference of place preferences and detection of dopamine release. The presented options for material and device integrations provide a practical route to simultaneous optical control and electrochemical sensing of complex nervous systems.

The solid phase thermal decomposition and nanocrystal effect are extremely important to understand the ignition, combustion, reaction growth and buildup to detonation under shock wave action. To explore the basic mechanism at the atomic level and understand the interaction among nanocrystal lattices, molecules, and intermediates during the solid phase decomposition, ReaxFF large-scale molecular dynamics simulation at 1000-3000 K was demonstrated on the solid phase of nanocrystalline RDX with a size in the range of 5-12 nm. Based on the analysis of the RDX decay and chemical species, we found that the whole decomposition process can be divided into the solid-affected stage and the following less-condensed phase stage. From the results of NO2 diffusion and high frequency reaction statistics for the nanocrystal effect on the RDX decay, intermediate diffusion was found to be strongly associated with the chemical pathway. In addition, it was found for the first time that the thermal decomposition of RDX originates from the inside of the nanocrystal instead of its surface. Furthermore, a promising uniform energy distribution mechanism transfer by vibration inside the nanocrystalline RDX was demonstrated. The detailed information derived from this study can aid in the thorough understanding of the size effect on the chemical kinetics of nanoexplosives, especially for thermal decomposition and reaction growth.

Medulloblastoma is the most common malignant brain tumor in children. Despite remarkable advances over previous decades, the long-term survival of patients with medulloblastoma remains poor due to the frequent metastatic nature of this malignancy. The aim of the present study was to examine the role of tripartite motif containing 59 (TRIM59) in cell metastasis in medulloblastoma. It was initially demonstrated that TRIM59 expression was significantly increased in clinical medulloblastoma tissues compared with adjacent non-cancerous tissues and differentially expressed in a series of medulloblastoma cell lines. The knockdown of TRIM59 in D283 cells resulted in epithelial-to-mesenchymal transition (EMT), and decreased cell migratory and invasive capacities. By contrast, the overexpression of TRIM59 in Daoy cells was able to inhibit the EMT process and increase migratory and invasive capacities of the cells. Notably, the knockdown of TRIM59 was able to decrease the protein level of matrix metalloproteinase (MMP)-2 without altering the levels of MMP-9, and conversely the overexpression of TRIM59 was able to increase the protein level of MMP-2. Importantly, the downregulation of TRIM59 in D283 cells was able to inhibit the levels of phosphorylated (p)-AKT (Ser473), glycogen synthase kinase 3 β(GSK3β; Ser9) and phosphoinositide 3-kinase (PI3K) p85 (Tyr458) without altering the levels of total protein. The data from the present study suggest that TRIM59 induces epithelial-to-mesenchymal transition and promotes migration and invasion by PI3K/AKT signaling pathway in medulloblastoma. This data may provide novel insight into tumor metastasis and pave the way for the development of therapeutic strategies for the treatment of medulloblastoma in the clinic.

A facile calcination method is developed for the in situ synthesis of nanohybrids of Ti

The present study aimed to investigate the mechanisms underlying microRNA (miRNA)-mediated regulation of chondrogenic differentiation. Mouse embryo-derived stem cells C3H10T1/2 were cultured and chondrogenic differentiation was induced using transforming growth factor-β3 (TGF-β3). In addition, miRNA expression profiles were detected via miRNA array analysis, and quantitative polymerase chain reaction was performed to verify the differentially expressed miRNAs. Furthermore, bioinformatics software was used to predict the putative targets and the prediction was validated by dual-luciferase reporter assays and western blot analysis. In addition, cell proliferation and glycosaminoglycans were measured by a direct cell count method and alcian blue staining, respectively. Compared with the control group, 86 miRNAs were identified as differentially expressed in TGF-β3-induced cells and the expression levels of 28 miRNAs were increased while the remaining 58 miRNAs exhibited a decline in expression. Amongst the differentially expressed miRNAs, miR-30b expression was observed to have significantly decreased during chondrogenic differentiation. SOX9 is a target gene of miR-30b, and miR-30b inhibits SOX9 expression during chondrogenic differentiation. Furthermore, the alcian blue staining results demonstrated that miR-30b inhibited early chondrogenic differentiation. However, the data of the present study indicated that miR-30b had no influence on C3H10T1/2 cell line proliferation. In conclusion, miR-30b is a key negative regulator of TGF-β3-induced C3H10T1/2 cell chondrogenic differentiation, which functions by directly targeting SOX9.