High-Temperature Superlubricity in MoS2/Graphene van der Waals Heterostructures.

Achieving high-temperature superlubricity is essential for modern extreme tribosystems. Solid lubrication is the sole viable alternative due to the degradation of liquid ones but currently suffers from notable wear, instability, and high friction coefficient. Here, we report robust superlubricity in MoS2/graphene van der Waals heterostructures at high temperatures up to ∼850 K, achieved through localized heating to enable reliable friction testing. The ultralow friction of the MoS2/graphene heterostructure is found to be notably further reduced at elevated temperature and dominantly contributed by the MoS2 edge. The observation can be well described by a multi-contact model, wherein the thermally activated rupture of edge-contacts facilitates the sliding. Our results should be applicable to other van der Waals heterostructures and shed light on their applications for superlubricity at elevated temperature.

ANKRD37 inhibits trophoblast migration and invasion by regulating the NF-κB pathway in preeclampsia.

BACKGROUND: Inadequate trophoblast invasion is associated with preeclampsia (PE). Ankyrin repeat domain protein 37 (ANKRD37) has been reported to be abnormally expressed in PE placentas. However, the role of ANKRD37 in trophoblasts has not been investigated. We aimed to determine the functions of ANKRD37 in PE and to explore the molecular mechanisms. METHODS: Here, fluorescence in situ hybridization, immunohistochemistry, Western blotting and quantitative real-time polymerase chain reaction were used to detect protein and mRNA expression levels. Cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, wound healing assay, transwell assay and RNA sequencing were performed to investigate the role of ANKRD37 and the underlying mechanism in HTR8/SVneo and JEG-3 cells, and extravillous explant cultures were used to evaluate the migration and invasion abilities of extravillous cytotrophoblasts. RESULTS: We found that ANKRD37 expression was upregulated in PE placentas compared to normal pregnancy placentas. ANKRD37 knockdown enhanced trophoblast migration and invasion, promoted extravillous explant outgrowth, and regulated the expression of key invasion proteins, whereas ANKRD37 overexpression exerted the opposite effects. RNA sequencing indicated that nuclear factor-kappa B (NF-κB) was the potential downstream pathway of ANKRD37, which was confirmed by the change in p-p65 and p-IκBα expression in JEG-3 and HTR8/SVneo cells. CONCLUSIONS: Our findings suggest that high expression of ANKRD37 inhibits trophoblast cell migration and invasion possibly via the NF-κB pathway, and may be related to the development of PE.

TOP2A deficit-induced abnormal decidualization leads to recurrent implantation failure via the NF-κB signaling pathway.

BACKGROUND: Successful implantation is a complex process that is influenced by embryo quality, endometrial receptivity, immune factors, and the specific type of in vitro fertilization protocol used. DNA topoisomerase IIα (TOP2A) is a well-known protein involved in cell proliferation; however, its expression and effect on the endometrium in recurrent implantation failure (RIF) have not been fully elucidated. METHODS: The human endometrial tissues of healthy controls and patients with RIF were collected. A proteomic analysis was performed to evaluate the differentially expressed proteins between the RIF group and the fertile control group. The expression patterns of TOP2A in the human preimplantation endometrium of the patients with RIF were determined by immunohistochemical staining, Western blotting and qRT-PCR. TOP2A knockdown (sh-TOP2A) T-HESCs were generated using lentiviruses. The expression of TOP2A in T-HESCs was manipulated to investigate its role in decidualization. The TOP2A-related changes in decidualization were screened by mRNA sequencing in decidualized TOP2A knockdown and control T-HESCs and then confirmed by Western blotting and immunofluorescence staining. TOP2A-deficient mice were generated by injection of TOP2A-interfering adenovirus on GD2.5 and GD3.5. RESULTS: We performed a proteomic analysis of endometrial tissues to investigate the potential pathogenesis of RIF by comparing the patients with RIF and the matched controls and found that TOP2A might be a key protein in RIF. TOP2A is ubiquitously expressed in both stromal and glandular epithelial cells of the endometrium. The data indicate that TOP2A expression is significantly lower in the mid-secretory endometrium of women with RIF. TOP2A expression was downregulated under stimulation by 8-bromo-cAMP and MPA. Ablation of TOP2A resulted in upregulated expression of decidual biomarkers and morphological changes in the cells. Mechanistic analysis revealed that TOP2A regulates the NF-κB signaling pathway in decidualized T-HESCs. The TOP2A-deficient mice exhibited lower fetal weights. CONCLUSIONS: Our findings revealed that abnormal expression of TOP2A affects decidualization and changes the "window of implantation", leading to RIF. TOP2A participates in the processes of decidualization and embryo implantation, functioning at least in part through the NF-κB pathway. Regulating the expression of TOP2A in the endometrium may become a new strategy for the prevention and treatment of RIF.

IL-23 skin and joint profiling in psoriatic arthritis: novel perspectives in understanding clinical responses to IL-23 inhibitors.

OBJECTIVES: To determine the relationship between synovial versus skin transcriptional/histological profiles in patients with active psoriatic arthritis (PsA) and explore mechanistic links between diseased tissue pathology and clinical outcomes. METHODS: Twenty-seven active PsA patients were enrolled in an observational/open-label study and underwent biopsies of synovium and paired lesional/non-lesional skin before starting anti-tumour necrosis factor (TNF) (if biologic-naïve) or ustekinumab (if anti-TNF inadequate responders). Molecular analysis of 80-inflammation-related genes and protein levels for interleukin (IL)-23p40/IL-23p19/IL-23R were assessed by real-time-PCR and immunohistochemistry, respectively. RESULTS: At baseline, all patients had persistent active disease as per inclusion criteria. At primary end-point (16-weeks post-treatment), skin responses favoured ustekinumab, while joint responses favoured anti-TNF therapies. Principal component analysis revealed distinct clustering of synovial tissue gene expression away from the matched skin. While IL12B, IL23A and IL23R were homogeneously expressed in lesional skin, their expression was extremely heterogeneous in paired synovial tissues. Here, IL-23 transcriptomic/protein expression was strongly linked to patients with high-grade synovitis who, however, were not distinguishable by conventional clinimetric measures. CONCLUSIONS: PsA synovial tissue shows a heterogeneous IL-23 axis profile when compared with matched skin. Synovial molecular pathology may help to identify among clinically indistinguishable patients those with a greater probability of responding to IL-23 inhibitors.

Effects of simvastatin on the expression of inducible nitric oxide synthase and brain-derived neurotrophic factor in a lipopolysaccharide-induced rat model of Parkinson disease.

OBJECTIVE: To investigate the effects of simvastatin on the expression of inducible nitric oxide synthase (iNOS) and brain-derived neurotrophic factor (BDNF) in the substantia nigra in a lipopolysaccharide (LPS)-induced rat model of Parkinson disease (PD), and to study the mechanisms underlying the neuroprotective effects of simvastatin in PD. METHODS: The LPS-PD model was established by injection of LPS (5 mg/mL, 2.0 µL) into the right substantia nigra compacta (SNC). Rats in the sham-operated group received saline. The simvastatin treatment group was intraperitoneally administered simvastatin (5 mg/kg, 2.0 µL) at 1 h before, and daily for 14 days after surgery, while the sham-operated and LPS-model groups received saline. Iba-1-positive cells and tyrosine hydroxylase (TH), as well as iNOS and BDNF in the SNC were detected by immunohistochemistry and Western blotting, respectively. The effect of simvastatin in the PD model was also examined in behavioral tests. RESULTS: The LPS-model group exhibited typical animal PD behaviors. Compared with the control group, the LPS-model group exhibited a decreased number of DA neurons (p < 0.01) in the SNC, as well as increases in the Iba-1-positive cell number and iNOS expression (p < 0.05), while BDNF expression was downregulated (p < 0.01). These effects were inhibited by simvastatin treatment (p < 0.05). CONCLUSION: Simvastatin mediates a protective effect on dopaminergic neurons in the SNC in the LPS-PD model, possibly by promoting neuronal repair and regeneration, and by inhibiting oxidative stress, thus improving substantia nigra function.

Deciphering the molecular landscape: integrating single-cell transcriptomics to unravel myofibroblast dynamics and therapeutic targets in clear cell renal cell carcinomas.

Background: Clear cell renal cell carcinomas (ccRCCs) epitomize the most formidable clinical subtype among renal neoplasms. While the impact of tumor-associated fibroblasts on ccRCC progression is duly acknowledged, a paucity of literature exists elucidating the intricate mechanisms and signaling pathways operative at the individual cellular level. Methods: Employing single-cell transcriptomic analysis, we meticulously curated UMAP profiles spanning substantial ccRCC populations, delving into the composition and intrinsic signaling pathways of these cohorts. Additionally, Myofibroblasts were fastidiously categorized into discrete subpopulations, with a thorough elucidation of the temporal trajectory relationships between these subpopulations. We further probed the cellular interaction pathways connecting pivotal subpopulations with tumors. Our endeavor also encompassed the identification of prognostic genes associated with these subpopulations through Bulk RNA-seq, subsequently validated through empirical experimentation. Results: A notable escalation in the nFeature and nCount of Myofibroblasts and EPCs within ccRCCs was observed, notably enriched in oxidation-related pathways. This phenomenon is postulated to be closely associated with the heightened metabolic activities of Myofibroblasts and EPCs. The Myofibroblasts subpopulation, denoted as C3 HMGA1+ Myofibroblasts, emerges as a pivotal subset, displaying low differentiation and positioning itself at the terminal point of the temporal trajectory. Intriguingly, these cells exhibit a high degree of interaction with tumor cells through the MPZ signaling pathway network, suggesting that Myofibroblasts may facilitate tumor progression via this pathway. Prognostic genes associated with C3 were identified, among which TUBB3 is implicated in potential resistance to tumor recurrence. Finally, experimental validation revealed that the knockout of the key gene within the MPZ pathway, MPZL1, can inhibit tumor activity, proliferation, invasion, and migration capabilities. Conclusion: This investigation delves into the intricate mechanisms and interaction pathways between Myofibroblasts and ccRCCs at the single-cell level. We propose that targeting MPZL1 and the oxidative phosphorylation pathway could serve as potential key targets for treating the progression and recurrence of ccRCC. This discovery paves the way for new directions in the treatment and prognosis diagnosis of ccRCC in the future.

Analyzing the relationship between the efficiency and safety of a turbo roundabout by the factor analysis method.

The construction of cities and economic development lead to more and more serious environmental pollution, and the concept of green and low-carbon city has been proposed. Therefore, a series of requirements have been put forward for transportation. CO and other pollutants will be produced in the exhaust of conventional fuel vehicles, which will seriously affect the urban environment, especially at intersections with large passenger and vehicle flows. When multiple roads, especially more than 4 roads, intersect on urban roads, traffic organization can usually be achieved by using a roundabout. However, due to the limited capacity of the conventional roundabout, with the rapid increase of the traffic volume, and there are many vehicles in the circle lane change and interweaving behavior. This has caused serious congestion at the roundabout, the significantly increase in pollutants emissions and the decline in air quality. As an unconventional design, the turbo roundabouts use canalized traffic to allowed drivers to select the appropriate lanes in advance depending on their destinations so that different lanes within the circle do not interfere with one another, which improves the safety of the intersection while ensuring capacity. The main purpose of this paper is to analyze the traffic efficiency and safety of the conventional roundabout scheme and turbo roundabout scheme for five-way intersections. Using VISSIM to simulate different forms of roundabout and analyzing the six selected evaluation indicators. The number of vehicles in different entrance lanes and the diameter of the circle are selected as sensitivity factors for sensitivity analysis. Finally, the factor analysis method (FAM) is used to classify the six indicators into two categories: traffic efficiency and traffic safety, so as to comprehensively evaluate the different schemes. The results show that the difference in performance between the two schemes was not significant at low traffic volumes. At high traffic volumes, the turbo roundabout was better than the conventional roundabout in terms of emissions, safety and throughput efficiency. CO emissions from vehicles on conventional roundabout are generally higher than those on turbo roundabout, up to 53.62%. Therefore, the turbo roundabout is more appropriate for heavy traffic conditions.

LINC01268 promotes epithelial-mesenchymal transition, invasion and metastasis of gastric cancer via the PI3K/Akt signaling pathway and targeting MARCKS.

BACKGROUND: Long non-coding RNAs (lncRNAs) with differential expression characteristics have been found to be closely related to the tumorigenesis and development of gastric cancer (GC), but their specific mechanisms and roles still need to be further elucidated. AIM: To investigate the expression of LINC01268 in GC and its mechanism of affecting GC progression. METHODS: Real-time quantitative polymerase chain reaction was used to detect the expression of LINC01268 in GC tissues, cell lines and plasma. The Kaplan-Meier method was used to evaluate the value of LINC01268 in the prognostication of GC patients. An receiver operating characteristic curve was constructed to evaluate the value of LINC01268 in the diagnosis of GC. Transwell migration and invasion assays and wound healing assays were used to confirm the effect of LINC01268 on the invasion and migration of GC cells. The regulatory relationship between LINC01268 and myristoylated alanine rich protein kinase C substrate (MARCKS), the PI3K/Akt signaling pathway, and the epithelial-mesenchymal transition (EMT) process in GC was demonstrated by western blot analysis. RESULTS: The expression of LINC01268 was increased in GC tissues and cell lines. The expression level of LINC01268 was significantly correlated with lymph node metastasis, TNM stage, and tumor differentiation in patients with GC. Over-expression of LINC01268 indicated a poor prognosis for patients with GC, and it had a certain auxiliary diagnostic value for GC. In vitro functional experiments proved that the abnormal expression of LINC01268 further activated the PI3K/Akt signaling pathway and promoted EMT by targeting and regulating MARCKS and ultimately promoted the invasion and metastasis of GC. CONCLUSION: This study elucidates that LINC01268 in GC may be an oncogene that further activates the PI3K/Akt signaling pathway and EMT by targeting and regulating MARCKS, and ultimately promotes the invasion and metastasis of GC. LINC01268 may be a potential effective target for the treatment of GC.

Functional role of the SLC7A11-AS1/xCT axis in the development of gastric cancer cisplatin-resistance by a GSH-dependent mechanism.

Resistance to platinum-based chemotherapy is a major obstacle in gastric cancer (GC) treatment. Abundant long noncoding RNAs (lncRNAs) are reported to play important roles in tumorigenesis and drug resistance biology. Herein, we report that the SLC7A11-AS1 and xCT are involved in cisplatin resistance in GC. SLC7A11-AS1 was downregulated and xCT was upregulated in cisplatin-resistant GC tissues and cell lines. GC patients with low expression of SLC7A11-AS1 and high expression of xCT had a poor prognosis and relatively poor response to chemotherapy. Overexpression of SLC7A11-AS1 weakened GC growth, reduced intracellular GSH biosynthesis, enhanced intracellular reactive oxygen species (ROS) and conferred sensitivity to cisplatin to resistant GC cells in vitro and in vivo. Mechanistically, SLC7A11-AS1 directly suppressed xCT expression, while miR-33a-5p remarkably reduced SLC7A11-AS1 and xCT expression by directly targeting the SLC7A11-AS1 and xCT 3'UTRs. In addition, we found that low SLC7A11-AS1 expression activated the p38MAPK-JNK signaling pathway, and increased the expression of cisplatin export gene ATP7A and the GSH biosynthesis gene GCLM in GC.

Cantharidin suppresses gastric cancer cell migration/invasion by inhibiting the PI3K/Akt signaling pathway via CCAT1.

Cantharidin (CTD) is a traditional Chinese medicine that shows an anticancer effects in multiple types of cancer cells. However, the mechanism of CTD anti-cancer function in gastric cancer (GC) is still unclear. The aim of the present study was to investigate the underlying mechanism that CTD inhibits proliferation and migration through suppression of the PI3K/Akt signaling. CTD induced GC cell apoptosis and inhibited metastasis measured by CCK8 assays as well as wound healing assays and transwell assays. Mechanistic investigations suggested that CTD modulated the PI3K/Akt signaling via western-blot and quantitative q-PCR. In addition, we identified and confirmed CCAT1 as a novel direct target of CTD inhibited PI3K/AKt signaling expression. In conclusion, our results provide new point into the critical role of CTD in suppressing PI3K/Akt signaling via down-regulation of CCAT1, resulting in suppression GC cell growth and migration/invasion.

Decreased expression of the long non-coding RNA HOXD-AS2 promotes gastric cancer progression by targeting HOXD8 and activating PI3K/Akt signaling pathway.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been shown to be associated with many tumors. However, the specific mechanism of lncRNAs in the occurrence and development of gastric cancer (GC) has not been fully elucidated. AIM: To explore the expression level and molecular mechanism of HOXD-AS2 in GC tissues and cells, and analyze its significance in the prognosis of GC. METHODS: Real-time quantitative PCR was used to detect the expression of HOXD-AS2 in 79 pairs of GC tissues and five cell lines. The pcHOXD-AS2 plasmid vector was constructed and transfected into SGC-7901 and SNU-1 GC cells. Matrigel Transwell and wound healing assays were used to confirm the effect of HOXD-AS2 on invasion and migration of GC cells. Cell counting kit-8 assay and flow cytometry were used to verify the effect of HOXD-AS2 on the proliferation, cell cycle, and apoptosis of GC cells. The relevant regulatory mechanism between HOXD-AS2 and HOXD8 and PI3K/Akt signaling pathway was verified by Western blot analysis. RESULTS: The low expression of lncRNA HOXD-AS2 was associated with lymph node metastasis and tumor-node-metastasis stage in GC. In vitro functional experiments demonstrated that overexpression of HOXD-AS2 inhibited GC cell progression. Mechanistic studies revealed that HOXD-AS2 regulated the expression of its nearby gene HOXD8 and inhibited the activity of the PI3K/Akt signaling pathway. CONCLUSION: These results indicate that downregulation of HOXD-AS2 significantly promotes the progression of GC cells by regulating HOXD8 expression and activating the PI3K/Akt signaling pathway. HOXD-AS2 may be a novel diagnostic biomarker and effective therapeutic target for GC.

Synthesis of Microporous Covalent Phosphazene-Based Frameworks for Selective Separation of Uranium in Highly Acidic Media Based on Size-Matching Effect.

On the basis of high stability of phosphorus-oxygen linkage, we constructed two microporous covalent phosphazene-based frameworks (CPFs), for the first time, by choosing hexachlorocyclotriphosphazene as a core unit and polyhydroxy aromatic compounds (hydroquinone or phloroglucinol) as monomers, named CPF-D and CPF-T, respectively. Characterization studies by using Fourier transform infrared, nuclear magnetic resonance, thermal gravimetric analysis, 60Co γ-ray irradiation, and so forth, demonstrated that both of the CPF materials have excellent acid and radiation stability and relatively higher thermal stability. The results of batch adsorption experiments show that CPF-T is significantly more capable of sorbing uranium than CPF-D. In a pure uranium system with higher acidity (pH 1), the uranium sorption amount of CPF-T can reach up to 140 mg g-1. Distinctively, in mixed-metal solution with 12 coexisting cations, CPF-T shows relatively stable and excellent uranium adsorption capability over a wide range of acidity (pH 4 to 3 M HNO3), and the difference in uranium sorption amounts is less than 30% with the maximum of 0.26 mmol g-1 at pH 4 and the minimum of 0.20 mmol g-1 at 3 M HNO3, which is far superior to that of the conventional solid-phase extractant (SPE) materials previously reported. The research results suggested that the sorption model based on the speculated mechanism of size-matching plus hydrogen bond network has played a dominant role in the process of uranium adsorption. The proposed strategy for the one-pot fabrication of an acid-resistant microporous framework materials by bridging the aromatic monomers via P-O bonds provides an alternative approach for the design and synthesis of new SPE materials with size-matching function desired for effective separation of uranium or other valuable metals from highly acidic environments.

The long non-coding RNA LINC01606 contributes to the metastasis and invasion of human gastric cancer and is associated with Wnt/ß-catenin signaling.

The dysregulation of long non-coding RNA (lncRNA) has increasingly been linked to human gastric cancer (GC). However, the LINC01606 expression level and clinical values, and its role in the molecular mechanism underlying GC remain largely unknown. In our research, we found that LINC010606 was elevated aberrantly and correlated with metastasis and invasion in GC patients. Moreover, we found that LINC01606 expression level was associated with Wnt/ß-catenin signaling. In addition, subsequent functional experiments showed that JW74, a specific Wnt/ß-catenin signaling inhibitor, inhibited the transcription of LINC01606 and suppressed migration and invasion in GC cell lines. We also revealed that LINC01606 might be associated with miR-423-5p to regulate the level to which the Wnt/ß-catenin signaling pathway is activated. In summary, the findings of this study, based on competing endogenous RNA (ceRNA) theory, combine new data on the interaction between miR-423-5p and Wnt3a and introduce LINC01606 as a new focus for research, thus providing new insight into possible molecular-level approaches to preventing the migration and invasion of GC.

Graphene-synergized 2D covalent organic framework for adsorption: A mutual promotion strategy to achieve stabilization and functionalization simultaneously.

Most of current absorbents are difficult to hold favorable stability and functionality simultaneously when used in condition of high acidity and strong radiation existing in nuclear industry. Herein, a new graphene-synergized 2D covalent organic framework (GS-COF) was obtained via an in-situ loading of a covalent organic framework (TDCOF) on graphene sheets based on a mutual promotion strategy proposed in this work. The corresponding oximation products, o-GS-COF, and also o-TDCOF as a reference object, were respectively prepared subsequently. The results of experiments confirmed that o-GS-COF possesses better acid and irradiation stability than that of o-TDCOF. Adsorption experiments showed that the adsorption capacity of o-GS-COF for uranium is 144.2 mg g-1, higher than that of GO (92.5 mg g-1) and o-TDCOF (105.0 mg g-1), and the maximum adsorption capacity reaches 220.1 mg g-1. In the multi-ions system, o-GS-COF also displayed good selective adsorption property for uranium with SFU/M 35-100 for 5 coexisting divalent metal ions and 14-18 for 5 coexisting trivalent lanthanide ions. The proposed strategy successfully achieved the synergistic improvement of both stability and functionality for the desired adsorbing materials and is of considerable practical utility in the field of design and preparation of reliable high-performance absorbents.

Targeted therapies: what they teach us about the pathogenesis of psoriasis and psoriatic arthritis.

INTRODUCTION: Biologic therapy has revolutionized treatment pathways in psoriatic joint and skin disease. It has also provided a useful tool with which pathological pathways of this condition may be explored. Areas covered: This review presents data on the clinical and biological effects of targeted therapy in psoriatic arthritis and psoriasis. Therapeutic agents covered include inhibitors of TNFα, inhibitors of the IL-23/IL-17 axis and inhibitors of intracellular small molecules involved in the transduction of the inflammatory signal. Trial data on clinical and imaging efficacy is reviewed in parallel with studies on biological effects at tissue level. Pathological insights gained from the use of these treatments are explored. Expert commentary: A close relationship exists between specific pathological types and clinical manifestations of psoriatic disease, including responses to treatment. Studying these relationships is likely to improve understanding of disease and enable rational selection of specific treatments for patients with specific pathotypes.

Decreased expression of the long non-coding RNA SLC7A11-AS1 predicts poor prognosis and promotes tumor growth in gastric cancer.

Many lncRNA and mRNA sense-antisense transcripts have been systematically identified in malignant cells. However, the molecular mechanisms of most lncRNA-mRNA pairs in gastric cancer remain largely unknown. We found the gastric cancer-associated lncRNA SLC7A11-AS1 and coding transcript mRNA SLC7A11 in human gastric cancer specimens by microarray. SLC7A11-AS1, antisense to SLC7A11, is significantly down-regulated in gastric cancer and could promote tumor growth in vitro and in vivo. The effects of SLC7A11-AS1 depend on the regulation of SLC7A11 via the ASK1-p38MAPK/JNK signaling pathway. These findings suggest that decreased expression of SLC7A11-AS1 contributes to the progression of gastric cancer and may be a novel diagnostic biomarker and effective therapeutic target in gastric cancer patients.

A New Biphenyl Neolignan from Leaves of Patrinia villosa (Thunb.) Juss.

RESULTS: One new stereoisomer of biphenylneolignan with four known compounds was isolated from the leaves of Patrinia villosa Juss. METHODS: The structure of the new compound was elucidated as 2,6,2',6'-tetramethoxy-4,4'-bis (1,2-trans-2,3-epoxy-1-hydroxypropyl) biphenyl (1) on the basis of spectroscopic analysis and comparison with literature data. The four known compounds were identified as 2,6,2',6'-tetramethoxy-4,4'-bis(1,2-cis-2,3-epoxy-1-hydroxypropyl)biphenyl (2), 1H-indole-3-carbaldehyde (3), luteolin (4) and quercetin(5) by comparison of their spectral data with the reported data, respectively. CONCLUSIONS: Compound 1 is a new biphenylneolignan, compound 2 and 3 were isolated for the first time from the plant. SUMMARY: One new stereoisomer of biphenylneolignan named 2,6,2',6'-tetramethoxy-4,4'-bis (1,2-trans-2,3-epoxy-1-hydroxypropyl) biphenyl with four known compounds was isolated from the leaves of Patrinia villosa Juss.

Preparation of carboxymethyl cellulose sulfates and its application as anticoagulant and wound dressing.

Tissue engineering is aiming to build an artificial environment or biological scaffold material that imitates the living environment of cells in the body. In this work, carboxymethyl cellulose sulfates were prepared by reacting carboxymethyl cellulose with N(SO3Na)3 which was synthesized by sodium bisulfite and sodium nitrite in aqueous solution. The reaction conditions affected the degree of substitution (DS) were measured by the barium sulfate nephelometry method. And the anticoagulant activity of carboxymethyl cellulose sulfates with different DS, concentration and molecular weights were investigated by the activated partial thromboplastin time (APTT), thrombin time (TT) and prothrombin time (PT). In addition, the effect of carboxymethyl cellulose sulfates on wound healing had been evaluated by the rate of wound healing and the histological examinations. The results indicated that the introduction of sulfate groups into the carboxymethyl cellulose sulfates improved its anticoagulant activity, and the wound dressings treated with carboxymethyl cellulose sulfates obviously promoted wound healing.

Modified dachengqi decoction combined with conventional treatment for treating acute exacerbation of chronic obstructive pulmonary disease: a systematic review based on randomized controlled trials.

Objective. This study intended to systematically evaluate the effectiveness and safety of modified Dachengqi Decoction (MDD) combined with conventional treatment for treating acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Method. An extensive search was performed within 6 English and Chinese electronic databases from inception to April 2012. Methodological quality was assessed according to Cochrane risk of bias assessment. Data were analyzed using Review Manager 5.1. Results. A total of 16 studies (involving 1112 patients) were included. The result showed that MDD and its modification combined with routine treatment were more effective in improving FEV1%pred, enhancing the significant effectiveness, reducing PCO2, and shortening duration of mechanical ventilation. Adverse events were reported in two trials with symptom of diarrhea, while no serious adverse effect was reported. Conclusion. Modified Dachengqi Decoction appears to be effective for treating AECOPD. However, more regular designed RCTs are needed because of insufficient methodological problems.

[Fusion expression of human renal cell carcinoma-associated antigen G250/MN/CA IX in prokaryotic expression system].

OBJECTIVE: To achieve high expression of human renal cell carcinoma-associated antigen G250 in Escherichia coli. METHODS: The gene fragments encoding the protein obtained by PCR was cloned into prokaryotic expression vector pET32a(+) and expressed in E. coli Rosseta. The immunogenicity of the recombinant protein was evaluated by Western blotting. RESULTS: The plasmid pET32a(+)/G250 was constructed and expressed in E. coli Rosseta successfully. Western blot analysis showed that the recombinant protein could be specifically recognized by monoclonal antibody M75. CONCLUSION: Efficient G250 expression is achieved in prokaryotic expression system, which may facilitate further functional study of the protein and its monoclonal antibody preparation.