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Photocatalytic syngas (CO and H2 ) production with CO2 as gas source not only ameliorates greenhouse effect, but also produces valuable chemical feedstocks. However, traditional photocatalytic systems require noble metal or suffers from low yield. Here, we demonstrate that S vacancies ZnIn2 S4 (VS -ZnIn2 S4 ) nanosheets are an ideal photocatalyst to drive CO2 reduction into syngas. It is found that building S vacancies can endow ZnIn2 S4 with stronger photoabsorption, efficient electron-hole separation, and larger CO2 adsorption, finally promoting both hydrogen evolution reaction (HER) and CO2 reduction reaction (CO2 RR). The syngas yield of CO and H2 is therefore significantly increased. In contrast to pristine ZnIn2 S4 , the syngas yield over VS -ZnIn2 S4 can be improved by roughly ≈4.73 times and the CO/H2 ratio is modified from 1:4.18 to 1:1. Total amount of syngas after 12 h photocatalysis is as high as 63.20 mmol g-1 without use of any noble metals, which is even higher than those of traditional noble metal-based catalysts in the reported literatures. This work demonstrates the critical role of S vacancies in mediating catalytic activity and selectivity, and highlights the attractive ability of defective ZnIn2 S4 for light-driven syngas production.

As a third-generation platinum drug, oxaliplatin (OX) is widely used as the first-line chemotherapeutic agent in the treatment of colorectal cancer (CRC). CRC cells acquire resistance to chemotherapy and develop resistance, which is a major challenge for the treatment of advanced CRC. Recent studies have suggested that the therapeutic resistance of tumors is affected by the tumor microenvironment (TME). As a critical role among TME, tumor-associated macrophages (TAMs) play an important role. However, their regulatory mechanism underlying the drug resistance in CRC remains largely unknown. In the present study, we found that the density of macrophages infiltrated into the CRC tissues from OX-resistant patients was significantly higher compared with the OX-sensitive patients. Interestingly, both the total N6-methyladenosine (m6A) RNA content and the expression of its critical methyltransferase METTL3 were increased in the CRC tissues from OX-resistant patients compared with the OX-sensitive patients. Furthermore, we demonstrated that the M2-polarized TAMs enabled the OX resistance via the elevation of METTL3-mediated m6A modification in cells. Through whole-genome CRISPR screening and further validation, we found that TRAF5 contributes to the METTL3-triggered OX resistance in CRC cells. This study unveiled that M2-TAMs were important mediators for the acquisition of OX resistance. Furthermore, we provided evidence that targeting of M2-TAMs and METTL3-mediated m6A modification might be a promising adjuvant therapeutic strategy for CRC patients, especially for OX-resistant CRC patients.

Objective. Iguratimod, a novel disease-modifying anti-rheumatic drug for the treatment of rheumatoid arthritis, has been approved in China and Japan. Here, we aimed to find whether iguratimod can inhibit the aggressive behavior and promote apoptosis of rheumatoid fibroblast-like synoviocytes (RA-FLSs). Methods. The proliferation of RA-FLSs was assessed by 5-ethynyl-2′-deoxyuridine test and Cell Counting Kit-8. Migration and invasion were determined by the wound test and a transwell assay. Apoptosis was tested by flow cytometry. The mRNA expression of matrix metalloproteinases (MMPs) and proinflammatory cytokines in RA-FLSs were measured by quantitative PCR and ELISA. To gain insight into the molecular signaling mechanisms, we determined the effect of iguratimod on the activation of mitogen-activated protein kinases (MAPK) signaling pathways by the cellular thermal shift assay (CETSA) and western blot. Results. Iguratimod treatment significantly reduced the proliferation, migration, and invasive capacities of RA-FLSs in a dose-dependent manner in vitro. MMP-1, MMP-3, MMP-9, Interleukin-6 (IL-6), and monocyte chemoattractant protein-1 mRNA and protein levels were all decreased after treatment with iguratimod. Furthermore, tumor necrosis factor-alpha- (TNF-α-) induced expression of phosphorylated c-Jun N-terminal kinases (JNK) and P38 MAPK were inhibited by iguratimod. Additionally, iguratimod promoted the apoptosis of RA-FLSs. Most importantly, iguratimod was shown to directly interact with JNK and P38 protein by CETSA assay. Moreover, activating transcription factor 2 (ATF-2), a substrate of both JNK and P38, was suppressed by iguratimod. Conclusions. Our findings suggested that the therapeutic effects of iguratimod on RA might be, in part, due to targeting the aggressive behavior and apoptosis of RA-FLSs.

To verify the positioning performance and reliability of multi-system combination Precise Point Positioning in landslide monitoring, we carried out a multi-system combination Precise Point Positioning calculation experiment on the monitoring data of a single landslide disaster area in Fujian Province. The coordinates of the monitoring points obtained by a continuously operating reference station and the monitoring station for static relative positioning were used as reference values. The GPS system was used as the standard system and the combined PPP solution mode of G/R/C, G/R/E and G/R/E/C was used to obtain the surface displacement of the landslide area. The research showed that multi-system combination PPP converges to the centimeter level in about 30 min. The average value of internal accordant precision was more than 1 mm after convergence, and that of the external accordant precision was more than 5 cm, which meets the centimeter-level accuracy requirements in rapid landslide deformation monitoring.

As a third-generation platinum drug, oxaliplatin (OX) is widely used as the first-line chemotherapeutic agent in the treatment of colorectal cancer (CRC). CRC cells acquire resistance to chemotherapy and develop resistance, which is a major challenge for the treatment of advanced CRC. Recent studies have suggested that the therapeutic resistance of tumors is affected by the tumor microenvironment (TME). As a critical role among TME, tumor-associated macrophages (TAMs) play an important role. However, their regulatory mechanism underlying the drug resistance in CRC remains largely unknown. In the present study, we found that the density of macrophages infiltrated into the CRC tissues from OX-resistant patients was significantly higher compared with the OX-sensitive patients. Interestingly, both the total

Tumor necrosis factor receptor-associated protein 1 (TRAP1), a member of the heat shock protein 90 (Hsp90) chaperone family, protects cells against oxidative stress and maintains mitochondrial integrity. To date, numerous studies have focused on understanding the relationship between aberrant TRAP1 expression and tumorigenesis. Mitochondrial TRAP1 is a key regulatory factor involved in metabolic reprogramming in tumor cells that favors the metabolic switch of tumor cells toward the Warburg phenotype. In addition, TRAP1 is involved in dual regulation of the mitochondrial apoptotic pathway and exerts an antiapoptotic effect on tumor cells. Furthermore, TRAP1 is involved in many cellular pathways by disrupting the cell cycle, increasing cell motility, and promoting tumor cell invasion and metastasis. Thus, TRAP1 is a very important therapeutic target, and treatment with TRAP1 inhibitors combined with chemotherapeutic agents may become a new therapeutic strategy for cancer. This review discusses the molecular mechanisms by which TRAP1 regulates tumor progression, considers its role in apoptosis, and summarizes recent advances in the development of selective, targeted TRAP1 and Hsp90 inhibitors.

The graphitic carbon nitride (g-C3N4) is regarded as a powerful support for constructing heterojunction. How to rationally design high-performance g-C3N4-based heterojunction remains a great challenge. In this work, a kind of spatial distribution heterojunction is prepared by in situ growing ZnIn2S4 (ZIS) nanosheets on g-C3N4 microtubes (T-CN). To highlight the advantage of such a structure design, g-C3N4 bulk (B-CN) and g-C3N4 nanosheets (S-CN) are also used as the supports to obtain B-CN/ZIS bulk heterojunction and S-CN/ZIS 2D/2D heterojunction, respectively. T-CN/ZIS spatial distribution heterojunction combines the hierarchical core/shell structure of B-CN/ZIS and ultrathin structure of S-CN/ZIS, which is much favorable for photocatalytic CO2 reduction. It is found that the gas yield from CO2 reduction is highest over T-CN/ZIS, which is 3.5 and 1.5 times higher than B-CN/ZIS and S-CN/ZIS. The experimental results manifest that the spatial distribution of ZIS nanosheets on T-CN induces stronger photoabsorption, faster interfacial charge transfer, and larger CO2 adsorption, all of which are responsible for the best catalytic activity. It is expected that this work will provide an instructive guideline for designing g-C3N4-based heterojunction.

The efficacy of traditional chemoradiotherapies for pancreatic cancer remains limited, and no effective targeted therapies or screening tests are currently available. Therefore more individualized drug screening is warranted for the clinical treatment of pancreatic cancer. A patient‑derived xenograft (PDX) model of pancreatic cancer bone metastasis was established, and next‑generation sequencing (NGS) was used to investigate the molecular characteristics of the cancer and screen for potential drugs. Immunohistochemical analysis was performed to validate that the PDX retained the molecular characteristics from the patient. Using NGS technology, 13 pancreatic‑cancer‑associated polymorphisms/mutations were identified out of 416 genes sequenced. Based on the sequencing results and associated literatures, AZD6244, a highly selective inhibitor against mitogen‑activated protein kinase kinase 1 (MEK1), was chosen as a potential therapy. AZD6244, a highly selective MEK1 inhibitor, was evaluated as effective for the pancreatic cancer PDX model, and thus may provide potential efficacy in the clinical treatment of the patient with pancreatic cancer investigated in the present study. The feasibility of the novel NGS‑PDX based drug‑screening pattern was demonstrated, and has a potential to improve individua-lized treatment for cancer.

The microstructure and texture evolution during linear friction welding (LFW) of pure titanium joints were investigated with scanning electron microscope, transmission electron microscope and electron back-scattering diffraction. The unique combination of high temperatures and strain rates during LFW causes limited continuous dynamic recrystallization in the weld center zone (WCZ), leading to a mixed microstructure of refined grains with severe elongated grains. Under the combined effect of axial pressure and shear stress, the texture across the weld line changes significantly. In parent metal, the c-axis of grains is parallel to the RD-TD plane and has an angle of 45° to TD, then in the thermomechanically affected zone the c-axis turns parallel to the welding interface and along the TD, finally in WCZ the c-axis turns to the ND and the P1 101¯0112¯0 texture forms. Compared with the ideal hcp shear textures, the present results show that material flow during LFW of titanium indeed arises from the simple-shear deformation and is governed by prismatic slip rather than twinning. The strong texture in LFWed joints is the cause of the anisotropic mechanical properties. Keywords: Linear friction welding, Titanium, Microstructure, Texture, Anisotropic mechanical properties

Effective therapies are limited for pancreatic cancer, particularly for those with distant tumour metastases. Therefore, more individualised drug screening is urgently required. Next-generation sequencing (NGS) is a powerful tool to investigate the genomic landscape of patients and the mechanism of drug response, which may provide a broader vision for potential clinical drug screening. Patient-derived xenograft (PDX) models may have a significant advantage in predicting clinical treatment response. In our previous study, a PDX of pancreatic cancer bone metastasis was established, and NGS was conducted to investigate the molecular information. In the present study, these data were further analysed and fibroblast growth factor receptor 1 (FGFR1) amplification was identified in a panel of 416 cancer-associated genes. Thus, AZD4547, an inhibitor against FGFR, was selected as a potential therapy, and was evaluated using the PDX model. AZD4547 was shown to exhibit antitumor activity by reducing the expression of FGFR1 and its targets. The present study also demonstrated the high potential of the novel NGS/PDX-based drug screening platform to improve individualised cancer treatment.

Polluted water and exhaust gas released from industrial activities cause a series of environmental issues such as heavy metals accumulation and greenhouse effect. Here, we have proposed an “adsorbent-to-photocatalyst” conversion strategy to bridge water remediation with photocatalytic CO2 reduction. Harmful heavy metals in polluted water are removed and collected by adsorbents, which are converted into valuable photocatalysts for CO2 reduction without secondary treatment. Calcium silicate hydrate (CSH) nanosheets are prepared as an ideal “bridge”. Their ultrathin thickness (2.8 nm), ultrahigh surface area (637.2 m2 g−1), and abundant surface hydroxyls are much favorable for both heavy metals removal and photocatalysis processes. Four typical heavy metals including Cu2+, Zn2+, Ni2+, and Pb2+ are selected for studies. Interestingly enough, in the case of Ni2+ removal, CSH nanosheets undergo phase change and they are spontaneously converted into a new semiconductor nickel silicate hydroxide. The nickel silicate hydroxide has a suitable energy level for reducing CO2 into CO. And its strong CO2 adsorption and abundant exposed Ni2+ sites contribute to efficient and selective photocatalytic CO2 reduction. The CO yield is up to 1.71 × 104 μmol g−1 h−1 with 99.2% selectivity under visible light.

The present work investigated the effects of the thermal cycles in air on the tensile properties of a 2.5 dimensional carbon fiber reinforced silicon carbide composite (2.5D-C/SiC) in weft and warp direction, prepared by low-pressure chemical vapor infiltration. The composite was exposed to different thermal cycles between 900 °C and 300 °C in air. The fracture morphologies of the failed composite were examined by a scanning electron microscope to investigate the underlying damage mechanisms. It is found that the composite can retain its tensile strength within 40 thermal cycles. Comparatively, the modulus of 2.5D-C/SiC decreases with increasing thermal cycles. Extensive pullout of fibers on the fractured surface and interface debonding suggest that the damage caused by the thermal cycles involves weakening of the bonding strength of coating/composite and fiber/matrix. The above damage supply the channel for the oxidation of PyC and carbon fibers in the composites.In addition, the degradation in warp direction is faster than that in weft direction.

Adipose-derived stem cells (ADSCs) were previously considered to have an anti-inflammatory effect, and Interleukin-1β (IL-1β) was found to be a pro-inflammatory factor in chondrocytes, but the mechanism underlying ADSCs and IL-1β is unclear. In this study, we investigate whether P2X7 receptor (P2X7R) signalling, regulated by microRNA 373 (miR-373), was involved in the ADSCs and IL-1β mediated inflammation in osteoarthritis (OA). Chondrocytes were collected from 20 OA patients and 20 control participants, and ADSCs were collected from patients who had undergone abdominal surgery. The typical surface molecules of ASDCs were detected by flow cytometry. The level of nitric oxide (NO) was determined by Griess reagent. Concentrations of prostaglandin E2 (PGE2), interleukin 6 (IL-6), matrix metallopeptidase 3 (MMP-3) were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of IL-6, MMP-3, miR-373 and P2X7R were determined by real-time polymerase chain reaction (PCR), and Western blot was used to detect the protein expression of P2X7R. The typical potential characters of ADSCs were verified. In chondrocytes or OA tissues, the miR-373 expression level was decreased, but the P2X7R expression was increased. IL-1β stimulation increased the level of inflammatory factors in OA chondrocytes, and ADSCs co-cultured with IL-1β-stimulated chondrocytes decreased the inflammation. OA chondrocytes transfected with the miR-373 inhibitor increased the inflammation level. The miR-373 mimic suppressed the inflammation by targeting P2X7R and regulated its expression, while its effect was reversed by overexpression of P2X7R. IL-1β induced inflammation in OA chondrocytes, while ADSCs seemed to inhibit the expression of P2X7R that was regulated by miR-373 and involved in the anti-inflammatory process in OA.

The prognosis of patients with osteosarcoma with distant metastasis and local recurrence remains poor. Increased expression of polymeric immunoglobulin receptor (pIgR) in tumor tissue has been detected in various types of cancer. However, the clinical significance of pIgR in osteosarcoma has yet to be elucidated. The present study aimed to investigate the prognostic value of pIgR in patients with osteosarcoma following surgical resection. pIgR expression was assessed using quantitative polymerase chain reaction analysis in cryopreserved osteosarcoma tissues from 22 patients, as well as using immunohistochemistry in paraffin-embedded osteosarcoma tissues from 136 patients. The association between pIgR expression, clinicopathological factors and long-term prognosis was retrospectively examined in these 136 patients. The prognostic significance of negative or positive pIgR expression in osteosarcoma was assessed using Kaplan-Meier survival analysis and log-rank tests. Univariate analysis indicated that patients with positive pIgR osteosarcoma tissue expression had a significantly worse overall survival (OS) compared with patients with negative pIgR osteosarcoma expression. Multivariate analysis revealed that positive pIgR expression in osteosarcoma tissues was an independent prognostic factor for OS following surgical resection (P

To reveal the shear properties of SiC matrix composites, interlaminar shear strength (ILSS) of three kinds of silicon carbide matrix composites was investigated by compression of the double notched shear specimen (DNS) at 900 °C in air. The investigated composites included a woven plain carbon fiber reinforced silicon carbide composite (2D-C/SiC), a two-and-a-half-dimensional carbon fiber-reinforced silicon carbide composite (2.5D-C/SiC) and a woven plain silicon carbon fiber reinforced silicon carbide composite (2D-SiC/SiC). A scanning electron microscope was employed to observe the microstructure and fracture morphologies. It can be found that the fiber type and reinforcement architecture have significant impacts on the ILSS of the SiC matrix composites. Great anisotropy of ILSS can be found for 2.5D-C/SiC because of the different fracture resistance of the warp fibers. Larger ILSS can be obtained when the specimens was loaded along the weft direction. In addition, the SiC fibers could enhance the ILSS, compared with carbon fibers. The improvement is attributed to the higher oxidation resistance of SiC fibers and the similar thermal expansion coefficients between the matrix and the fibers.

The tension –tension fatigue properties were investigated for a 2.5D-C/SiC composite in warp and weft direction. The fatigue experiments were carried out at room temperature (RT) and 900 C in laboratory air. The tensile properties of the specimens survived 10 6 cycles were determined to explore the damage mechanisms. The fracture surfaces were examined by a scannin g electron mic roscope. The composite exhib its excellent fatigue resistance at RT. The fatigue limits in both directions are about 85% of the ultimate tensile strength. The tensile stren gth and failure strain of the C/SiC can be enhanced for the survived comp osite at RT. The fatigue limits of the composite at 900 C are much lower than those at RT in both directions . Examination of the fracture surfaces revealed that the failure is closely related to the propagation of the cracks originated from the crossover of the bundles and produc ed within the bundles. The cracks also offered the chan nels for the oxygen to penetrate into the composite and are responsible for the oxidization of the carbon fibers in the composite. The oxidization of the fibers plays a critical key role in decreasing the fatigue limits at 900 C.

The thermal shock properties of a two-dimensional carbon fiber-reinforced silicon carbide composite with a multilayered self-healing coating (2D-C/SiC) were investigated in air. The composite was prepared by low-pressure chemical vapor infiltration. 2D-C/SiC specimens were thermally shocked for different cycles between 900 and 300 °C. The thermal shock resistance was characterized by residual tensile properties and mass variation. The change of the surface morphology and microstructural evolution of the composite were examined by a scanning electron microscope. In addition, the phase evolution on the surfaces was identified using an X-ray diffractometer. It is found that the composite retains its tensile strength within 20 thermal shock cycles. However, the modulus of 2D-C/SiC decreases gradually with increasing thermal shock cycles. Extensive pullout of fibers on the fractured surface and peeling off of the coating suggest that the damage caused by the thermal shock involves weakening of the bonding strength of coating/composite and fiber/matrix. In addition, the carbon fibers in the near-surface zone were oxidized through the matrix cracks, and the fiber/matrix interfaces delaminated when the composite was subjected to a larger number of thermal shock cycles.

The clinical relevance of frizzled-related protein (FRZB) in hepatocellular carcinoma (HCC) bone metastasis remains uncertain. The aim of this study was to assess the clinical relationship of FRZB in patients with HCC bone metastasis after surgical resection. FRZB expression was evaluated by immunohistochemistry in formalin-fixed paraffin embedded (FFPE) HCC and paired bone metastasis tissues from 13 patients that underwent surgical resection. The clinical characteristics of 13 HCC patients with synchronous or metachronous bone metastasis received surgery were retrospectively reviewed. We found that FRZB was positive in 9 HCC tissues (69.2%) and in 11 paired bone metastatic tissues (84.6%) among these 13 paired samples. The expression of FRZB in the bone metastases was noticeably higher than that in the paired HCC tissues. The expression of FRZB was up-regulated in 10 (76.9%) paired bone metastases tissues. FRZB expression was up-regulated in HCC bone metastasis tissue, which suggested that FRZB might play a key role in the HCC bone metastasis.

The nervous system plays an important role in the regulation of epithelial homeostasis and has also been postulated to play a role in tumorigenesis. Perineural invasion (PNI) is the only interaction between cancer cells and nerves studied to date. It is a symbiotic relationship between cancer cells and nerves that result in growth advantage for both. The potential association between HCC bone metastases and PNI is unknown. In this study, we investigate the nerve density in HCC and paired bone metastases to reveal the potential association of HCC bone metastases and PNI. The nerve density was evaluated by immunohistochemistry in formalin-fixed paraffin embedded (FFPE) hepatocellular carcinoma (HCC) and paired bone metastases tissues from 13 HCC patients with synchronous or metachronous bone metastases that underwent surgical resection. FFPE specimens of HCC bone metastases tissues express higher perineural density than HCC tissues, pointing to a potential role of the PNI in bone metastases from HCC. This is the first description of the potential association of PNI and HCC bone metastases.

OBJECTIVE: Minimally invasive midvastus approach (mini-midvastus) has been widely used in total knee arthroplasty (TKA). However, the clinical effects still remains controversial. This meta-analysis was based on randomized controlled trials (RCTs) aiming to quantitatively analyze the clinical efficacy of mini-midvastus versus standard parapatellar approach in TKA. METHODS: This meta-analysis was performed according to the PRISMA guidelines. A literature search for the eligible RCTs was carried out in the databases of PubMed, the Cochrane library, EMBASE and Web of Science. Two independent reviewers independently completed the study selection, data extraction, and the assessment of methodological quality. Meta-analysis was conducted by the RevMan 5.2 software. RESULTS: A total of 18 RCTs (937 patients with 1093 TKAs) published from 2007 to 2013 were included. The meta-analysis suggested that the mini-midvastus approach significantly improved knee range of motion (ROM) and decreased visual analog score (VAS) at postoperative 1-2 weeks (p0.05). However, the operative time was significantly longer when performing the mini-midvastus group than the parapartellar approach (p