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Background: This study aimed to evaluate the efficacy and safety of high-dose dual therapy for Helicobacter pylori (H. pylori) eradication compared to bismuth-containing quadruple therapy., Methods: The electronic database of PubMed, Embase, and Cochrane Library were searched from inception to March 18, 2021. Randomized, controlled trials that evaluated high-dose dual therapy versus bismuth-containing quadruple therapy for H. pylori infection were included., Results: We included 6 studies containing 1677 patients with H. pylori infection. This meta-analysis demonstrated that high-dose dual therapy achieved similar eradication rate compared with bismuth-containing quadruple therapy (intention-to-treat: 84.6% vs 83.7%, relative risk (RR) = 1.01, 95% CI: 0.97-1.06, P = .49; per-protocol = 88.4% vs 89.0%, RR = 1.00, 95% CI: 0.97-1.04, P = .99). However, highdose dual therapy showed fewer side effects (13.1% vs 32.0%, RR = 0.51, 95% CI: 0.34-0.78, P = .002) and better compliance (96.1% vs 93.3%, RR = 1.03, 95% CI: 1.00-1.05, P = .03) compared to bismuth-containing quadruple therapy., Conclusion: This meta-analysis demonstrated that high-dose dual therapy is equally effective with bismuth-containing quadruple therapy in eradicating H. pylori, with fewer side effects and better compliance.

Rational design, controllable synthesis, and an in-depth mechanism study of Cu-based bifunctional semiconductor heterostructures toward overall water splitting (OWS) are imperative but still face challenges. Herein, n-type iron oxide and p-type nickel phosphide and cobalt phosphide are respectively coupled with p-type cuprous phosphide nanowires on Cu foams via a general growth-phosphorization strategy. These self-supported semiconductor heterojunctions with different built-in potentials ( E BI ) are used as binder-free electrodes for OWS and exhibit significantly improved electrocatalytic activities compared to their counterparts. Among them, the heterostructure with the largest E BI of 1.57 V attains the smallest overpotential of 97 mV at 10 mA cm -2 for the hydrogen evolution reaction and 243 mV at 50 mA cm -2 for the oxygen evolution reaction in 1 M KOH. The corresponding two-electrode electrolyzer requires a cell voltage of 1.685 V at 50 mA cm -2 and shows admirable long-term stability at 100 mA cm -2 with a Faraday efficiency of around 98%. These promoted electrocatalytic performances originate from the enhanced active site, accelerated charge transfer, enlarged electrochemical active surface area, and synergy between different components at the heterointerface. This work represents a promising avenue to construct cost-efficient semiconductor heterostructures as bifunctional electrocatalysts applied to the sustainable energy industry.

Advanced gastric cancer (GCa) remains highly lethal due to the lack of effective therapies. Identifying promising therapeutic targets and developing effective treatment against GCa are urgently needed. Through mRNA and protein analysis of GCa clinical tumor samples, we found that autophagy-related gene 4B (ATG4B) was overexpressed in GCa tumors and that its high expression was associated with patients' poor prognosis. Knockdown of ATG4B significantly inhibited GCa cell survival and tumor growth. To further probe the role of ATG4B in GCa by pharmacological means, we screened an in-house marine natural compound library against ATG4B and identified Azalomycin F4a (Am-F4a) as a novel and potent ATG4B inhibitor. Am-F4a directly bound to ATG4B with high affinity and effectively suppressed GCa cell autophagy via inhibition of ATG4B both in vitro and in vivo. Moreover, Am-F4a or ATG4B knockdown significantly suppressed tumor growth as well as GCa cell migration and invasion. Am-F4a effectively blocked the metastatic progression of primary GCa and sensitized tumors to chemotherapy. Taken together, our findings indicate that ATG4B is a potential therapeutic target against GCa and the natural product Am-F4a is a novel ATG4B inhibitor that can be further developed for the treatment of GCa., (© 2022. The Author(s).)

Clear cell renal cell carcinoma (ccRCC) is a fatal cancer of the urinary system. Long non-coding RNAs (lncRNAs) act as competitive endogenous RNAs (ceRNAs) involving the ccRCC progression. However, the relationship between the ceRNA network and immune signature is largely unknown. In this study, the ccRCC-related gene expression profiles retrieved from the TCGA database were used first to identify the differentially expressed genes through differential gene expression analysis and weighted gene co-expression network analysis. The interaction among differentially expressed lncRNAs, miRNAs, and mRNAs were matched using public databases. As a result, a ceRNA network was developed that contained 144 lncRNAs, 23 miRNAs, as well as 62 mRNAs. Four of 144 lncRNAs including LINC00943, SRD5A3-AS1, LINC02345, and U62317.3 were identified through LASSO regression and Cox regression analyses, and were used to create a prognostic risk model. Then, the ccRCC samples were divided into the high- and low-risk groups depending on their risk scores. ROC curves, Kaplan-Meier survival analysis, and the survival risk plots indicated that the predictive performance of our developed risk model was accurate. Moreover, the CIBERSORT algorithm was used to measure the infiltration levels of immune cells in the ccRCC samples. The further genomic analysis illustrated a positive correlation between most immune checkpoint blockade-related genes and the risk score. In conclusion, the present findings effectually contribute to the comprehensive understanding of the ccRCC pathogenesis, and may offer a reference for developing novel therapeutic and prognostic biomarkers.

Thermoelectric materials are promising for energy harvesting using waste heat. The thermal management of the thermoelectric materials attract scientific and technological interests. The narrow bandgap semiconductor BiAgSe 2 is a good candidate for thermoelectric materials due to its ultralow thermal conductivity. The mother compound BiAgSe 2 crystallizes in hexagonal symmetry at room temperature, but experiences structural transitions to cubic phase at high temperature. By contrast, the daughter compound BiAgSeTe exhibits long range ordering and crystallizes into cubic phase at room temperature. Nevertheless, the local structural disorderings due to the Bi 3+ and Ag + anti-site defects, as well as local structural distortions, are ubiquitous in both parent BiAgSe 2 and BiAgSeTe. BiAgSeTe exhibits distinct transport properties owing to the disordering-induced drastic changes in the electronic band structure, as well as the scattering dictated by the point defects. It is suggested that BiAgSe 2 and BiAgSeTe could be good candidates for phonon glass and crystal glass (PGEC)-type thermoelectrics.

Background: Long noncoding RNAs (lncRNAs) play a central role in the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). TMPO antisense RNA 1 (TMPO-AS1) has been reported in many tumors. Nevertheless, the underlying mechanism whereby TMPO-AS1 influences HCC remains unclear. Our research aimed to reveal the molecular mechanism governing the function of TMPO-AS1 in HCC., Methods: TMPO-AS1 expression levels in HCC tissues/cells were evaluated using reverse transcriptase-polymerase chain reaction. The effect of TMPO-AS1 on the progression of HCC was observed by Cell Counting Kit-8 (CCK8), clone formation, wound healing, and transwell. The direct interaction between TMPO-AS1 and microRNA (miR)-126-3p was observed using a dual-luciferase reporter., Results: We found TMPO-AS1 expression to be remarkably higher in HCC specimens and associated with poor prognosis. Silencing of TMPO-AS1 not only inhibited HCC cell proliferation but also significantly reduced epithelial-to-mesenchymal transition-induced invasion and migration to a remarkable degree. According to the results from the online database analysis tools implemented to identify if TMPO-AS1 could target miR-126-3p, we found that miR-126-3p had a negative relationship with TMPO-AS1 in HCC specimens. Meanwhile, the luciferase reporter assay confirmed that TMPO-AS1 could directly act on miR-126-3p. Moreover, the silencing of miR-126-3p dramatically abolish the inhibitive influence of sh-TMPO-AS1 on HCC development., Conclusions: Our research demonstrated that TMPO-AS1 acts as a sponge for the tumor suppressor miR-126-3p in HCC and promotes the expression of LRP6 indirectly. Taken together, our results show that TMPO-AS1 may be regarded as a novel therapeutic target in the treatment of liver cancer., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/atm-21-5593). The authors have no conflicts of interest to declare., (2021 Annals of Translational Medicine. All rights reserved.)

A multi-purpose in operando optical cell with temperature and gas pressure control is described. This device allows for in operando Raman spectroscopy measurements for different applications. Its original design includes a temperature control from room temperature up to 1000°C and a heating stage that provides uniform and stable thermal conditions. The pressure control of the cell ranges from 10 -1  Pa to 6 MPa, and it is compatible with different gases. Both oxidizing and reducing gases are allowed to pass through the sample surface under study. The device has been calibrated and applied to collect Raman spectra for different reaction systems under various operating temperatures and pressures.

The Polycomb protein enhancer of zeste homolog 2 (EZH2) has critical roles in prostate cancer (PCa) progression and drug-resistance, which remains an obstacle for PCa treatment. Enzalutamide (ENZ) is a second-generation androgen receptor antagonist employed for treatment of metastatic castration-resistant prostate cancer A considerable proportion of tumors eventually develop resistance during treatment. Thus, agents that can overcome resistance to PCa are needed urgently. Ilicicolin A (Ili-A), an ascochlorin derivative isolated from the coral-derived fungus Acremonium sclerotigenum GXIMD 02501, shows antiproliferative activity in human PCa cells, but its mechanism of action against Castration-resistant prostate cancer is not known. Herein, RNA-sequencing showed the EZH2 pathway to be involved in PCa proliferation. Ili-A at low doses reduced the protein level of EZH2, leading to transcriptional change. Interestingly, Ili-A suppressed the binding of EZH2 to promoter regions in AR/serine/threonine polo-like kinase-1/aurora kinase A. Moreover, Ili-A could enhance the anticancer activity of enzalutamide in CRPC cancer models. These data suggest that Ili-A could be used in combination with enzalutamide to treat CRPC., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Guo, Luo, Yang, Zhang, Huang, Wang, Guo, Huang, Chen, Wang, Wang, Lei, Xiang and Liu.)

Drug-induced liver injury (DILI) caused by the ingestion of medications, herbs, chemicals or dietary supplements, is a clinically widespread health problem. The underlying mechanism of DILI is the formation of reactive metabolites, which trigger mitochondrial oxidative stress and the opening of mitochondrial permeability transition (MPT) pores through direct toxicity or immune response, leading to cell inflammation, apoptosis, and necrosis. Traditionally, mitochondria play an indispensable role in maintaining the physiological and biochemical functions of cells by producing ATP and mediating intracellular signal transduction; drugs can typically stimulate the mitochondria and, in the case of sustained stress, can eventually cause impairment of mitochondrial function and metabolic activity. Meanwhile, the mitochondrial stress response, as an adaptive protective mechanism, occurs when mitochondrial homeostasis is threatened. In this review, we summarize the relevant frontier researches of the protective effects of mitochondrial stress response in DILI as well as the potential related mechanisms, thus providing some thoughts for the clinical treatment of DILI., (© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)

Background: Clinicians in intensive care units (ICUs) have been prioritized for COVID-19 vaccination. We aim to understand the reasons behind vaccination refusal, and assess preferences for COVID-19 vaccines among Chinese ICU clinicians., Research Design and Methods: ICU clinicians throughout China's mainland were contacted to participate in an online survey. We compared concerns with vaccination status, and through a discrete choice experiment (DCE) assessed preferences for vaccines in terms of effectiveness, risk of adverse reactions, duration of immunity, and whether coworkers have been vaccinated., Results: Among 11,951 ICU respondents from 252 prefecture-level regions, vaccination coverage was 75.4%, with an additional 9.2% not vaccinated but intending to, and 16.1% not vaccinated and not intending to. ICU clinicians not intending to be vaccinated significantly expressed more concerns about the speed of vaccine development (30.1%) and adverse reactions (65.9%). In the DCE, the only significant difference in preferences of a COVID-19 vaccine was for safety, with those not intending to have a stronger preference for a vaccine with fewer adverse reactions (OR = 4.49), compared to those already vaccinated (OR = 2.90) or those intending to vaccinate (OR = 3.46)., Conclusion: Increasing vaccination coverage among Chinese ICU clinicians will require strong norms surrounding vaccination and transparency about safety information.

Human dihydroorotate dehydrogenase ( h DHODH) is an attractive tumor target essential to de novo pyrimidine biosynthesis. Novel potent h DHODH inhibitors with low toxicity are urgently needed. Herein, we demonstrate the isolation of 25 ascochlorin (ASC) derivatives, including 13 new ones, from the coral-derived fungus Acremonium sclerotigenum , and several of them showed pronounced inhibitions against h DHODH and triple-negative breast cancer (TNBC) cell lines, MDA-MB-231/-468. Interestingly, we found that h DHODH is required for proliferation and survival of TNBC cells, and several ASCs significantly inhibited TNBC cell growth and induced their apoptosis via h DHODH inhibition. Furthermore, the novel and potent h DHODH inhibitors ( 1 and 21 ) efficiently suppressed tumor growth in patient-derived TNBC xenograft models without obvious body weight loss or overt toxicity in mice. Collectively, our findings offered a novel lead scaffold as the h DHODH inhibitor for further development of potent anticancer agents and a potential therapeutic strategy for TNBC.

Background: microRNAs (miRNAs) have been shown to significantly contribute to the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). Specifically, miR-744-5p has been shown to be associated with tumor development, but the underlying mechanism by which miR-744-5p affects HCC remains unclear. Thus, this study sought to explore the molecular mechanism governing the function of miR-744-5p in HCC., Methods: The expression of miR-744-5p in HCC tissues/cells was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Colony-formation, cell-counting kit 8 (CCK-8), Transwell, and wound-healing assays were used to assess the proliferation and metastasis of HCC cells. Additionally, the interaction between miR-744-5p and transforming growth factor-beta 1 (TGF-β1) was detected using a dual-luciferase reporter and a Western-blot analysis., Results: miR-744-5p expression was shown to be significantly reduced in HCC tissues and cells. The overexpression of miR-744-5p not only significantly inhibited HCC cell proliferation, but also significantly reduced epithelial-mesenchymal transition-induced invasion. A luciferase reporter assay validated the ability of miR-744-5p to directly target TGF-β1. Further, the overexpression of TGF-β1 appeared to abolish the inhibitive effect of miR-744-5p mimics on HCC development., Conclusions: As per our findings, it was revealed that miR-744-5p suppresses HCC proliferation and invasion by regulating the TGF-β1 signaling pathway and epithelial-mesenchymal-transition (EMT)., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/jgo-21-319). The authors have no conflicts of interest to declare., (2021 Journal of Gastrointestinal Oncology. All rights reserved.)

Superlubricity is a fascinating phenomenon which attracts people to continuously expand ultralow friction and wear from microscale to macroscale. Despite the impressive advances in this field, it is still limited to specific materials and extreme operating conditions. Introducing a heterostructure with intrinsic lattice mismatch into delicate topologies mimicked from nature provides a promising alternative toward macroscopic superlubricity. Herein, 3D-printed MoS 2 /MoSe 2 heterostructures with bioinspired circular-cored square/hexagonal honeycomb topologies were developed. Compared to 3D-printed Al 2 O 3 , all topological structures with both high hardness and excellent flexural strength achieve more than 30% decrease in the friction coefficient. The circular-cored hexagonal honeycomb composite with 30% area density exhibits a stable ultralow friction coefficient of 0.09 and a low wear rate of 2.5 × 10 -5 mm 3 ·N -1 m -1 under 5 N. Even under 10 N, a highly desirable coefficient value of 0.08 can be maintained within 370 s. The extraordinary ultralow friction could be attributed to the small contact area, high lubricant mass loading, efficient collection and storage of both abrasive debris and lubricant, and the self-orientation in the lubricating film. This work provides new insights into developing high-efficiency lubrication devices and aids in the industrial application of macroscopic superlubricity in future life.

Acute lung injury induced by ischemia-reperfusion (I/R)-associated pulmonary inflammation is associated with high rates of morbidity. Despite advances in the clinical management of lung disease, molecular therapeutic options for I/R-associated lung injury are limited. Zinc finger protein 36 (ZFP36) is an AU-rich element-binding protein that is known to suppress the inflammatory response. A ZFP36 binding site occurs in the 3' UTR of the cAMP-response element-binding protein (CREB) binding protein (CREBBP) gene, which is known to interact with apoptotic proteins to promote apoptosis. In this study, we investigate the involvement of ZFP36 and CREBBP on I/R-induced lung injury in vivo and in vitro. Intestinal ischemia/reperfusion (I/R) activates inflammatory responses, resulting in injury to different organs including the lung. Lung tissues from ZFP36-knockdown mice and mouse lung epithelial (MLE)-2 cells were subjected to either Intestinal I/R or hypoxia/reperfusion, respectively, and then analyzed by Western blotting, immunohistochemistry, and real-time PCR. Silico analyses, pull down and RIP assays were used to analyze the relationship between ZFP36 and CREBBP. ZFP36 deficiency upregulated CREBBP, enhanced I/R-induced lung injury, apoptosis, and inflammation, and increased I/R-induced lung fibrosis. In silico analyses indicated that ZFP36 was a strong negative regulator of CREBBP mRNA stability. Results of pull down and RIP assays confirmed that ZFP36 direct interacted with CREBBP mRNA. Our results indicated that ZFP36 can mediate the level of inflammation-associated lung damage following I/R via interactions with the CREBBP/p53/p21/Bax pathway. The downregulation of ZFP36 increased the level of fibrosis.

Among several leading cardiovascular disorders, ischemia-reperfusion (I/R) injury causes severe manifestations including acute heart failure and systemic dysfunction. Recently, there has been increasing evidence suggesting that alterations in mitochondrial morphology and dysfunction also play an important role in the prognosis of cardiac disorders. Long non-coding RNAs (lncRNAs) form major regulatory networks altering gene transcription and translation. While the role of lncRNAs has been extensively studied in cancer and tumor biology, their implications on mitochondrial morphology and functions remain to be elucidated. In this study, the functional roles of Zinc finger protein 36-like 2 (ZFP36L2) and lncRNA PVT1 were determined in cardiomyocytes under hypoxia/reoxygenation (H/R) injury in vitro and myocardial I/R injury in vivo. Western blot and qRT-PCR analysis were used to assess the levels of ZFP36L2, mitochondrial fission and fusion markers in the myocardial tissues and cardiomyocytes. Cardiac function was determined by immunohistochemistry, H&E staining, and echocardiogram. Ultrastructural analysis of mitochondrial fission was performed using transmission electron microscopy. The mechanistic model consisting of PVT1 with ZFP36L2 and microRNA miR-21-5p with E3 ubiquitin ligase MARCH5 was assessed by subcellular fraction, RNA pull down, FISH, and luciferase reporter assays. These results identified a novel regulatory axis involving PVT1, miR-21-5p, and MARCH5 that alters mitochondrial morphology and function during myocardial I/R injury. Using an in vivo I/R injury mouse model and in vitro cardiomyocytes H/R model, we demonstrated that ZFP36L2 directly associates with PVT1 and alters mitochondrial fission and fusion. PVT1 also interactes with miR-21-5p and suppresses its expression and activity. Furthermore, we identified MARCH5 as a modifier of miR-21-5p, and its effect on mitochondrial fission and fusion are directly proportional to PVT1 expression during H/R injury. Our findings show that manipulation of PVT1-miR-21-5p-MARCH5-mediated mitochondrial fission and fusion via ZFP36L2 may be a novel therapeutic approach to regulate myocardial I/R injury.

Background: The discovery of checkpoint inhibitors towards cytotoxic T-lymphocyte protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) has been revolutionary for the treatment of cancers. These therapies have only offered an average of 20%-30% response rates across the tumor spectrum and the combination of agonists towards the tumor-necrosis superfamily members, such as 4-1BB and CD40, has shown potent efficacy in preclinical studies; however, these agonists have exhibited high degrees of toxicity with limited efficacy in human trials. In this study, we have generated a single-domain antibody towards a unique epitope of 4-1BB that limits its potential on-target toxicity while maintaining sufficient potency. This 4-1BB binder is ideal for use in the engineering of multispecific antibodies to localize 4-1BB activation within the tumor microenvironment, as shown here by a anti-PD-L1/4-1BB bispecific candidate (PM1003)., Methods: To determine the functional activity of the 4-1BB- and PD-L1-binding elements of PM1003, in vitro luciferase reporter and primary cell assays were used to test the potency of programmed cell death 1 ligand 1 (PD-L1) blockade and PD-L1-mediated 4-1BB activation via cross-bridging. X-ray crystallography was conducted to resolve the binding epitopes of the respective binding arms, and accurate binding kinetics were determined using standard affinity measurement techniques. Human 4-1BB and/or PD-L1 knock-in mice were used in cancer models for testing the in vivo antitumor efficacy of PM1003, and safety was evaluated further., Results: PM1003 shows potent activation of 4-1BB and blockade of PD-L1 in cell-based assays. 4-1BB activation was exerted through the bridging of PD-L1 on target cells and 4-1BB on effector cells. No PD-L1-independent activation of 4-1BB was observed. Through X-ray crystallography, a unique binding epitope in the cysteine-rich domain 4 (CRD4) region was resolved that provides high potency and potentially low on-target toxicity as determined by primary immune cell assays and toxicity evaluation in vivo ., Conclusions: A unique single-domain antibody was discovered that binds to the CRD4 domain of 4-1BB. When incorporated into a 4-1BB/PD-L1 bispecific (PM1003), we have shown the potent inhibition of PD-L1 activity with 4-1BB agonism upon cross-bridging with PD-L1 in vitro . Antitumor activity with minimal toxicity was found in vivo . Thus, PM1003 is a uniquely differentiating and next generation therapeutic agent for cancer therapy., Competing Interests: Competing interests: The research was funded by Biotheus Inc. All authors are current employees of Biotheus. Inc, with the exception of JZ, TZ and BL who declare no competing interests., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Liver ischemia/reperfusion injury (IRI), a serious inflammatory response driven by innate immunity, occurs in liver surgeries such as liver resection and liver transplantation, leading to liver dysfunction, liver failure, and even rejection after transplantation. Liver kinase B1 (LKB1) plays a pivotal anti-inflammatory role in IRI. One of the most important factors involved in liver IRI is the aberrant activation of the nucleotide binding oligomerization domain like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome in Kupffer cells. However, the mechanisms underlying the effect of LKB1 on the NLRP3 inflammasome in liver IRI remain elusive. In this study, we found that the expression of LKB1 was decreased in liver IRI, while the NLRP3 inflammasome level was increased as shown, as revealed by RT-qPCR and western blot analysis. Furthermore, upregulation of LKB1 abrogated the expression of the NLRP3 inflammasome, which improved liver function and liver pathology in the liver IRI model in vivo. In vitro, overexpression of LKB1 inhibited the activation of NLRP3 inflammasome and nuclear factor-κB, while the inhibitory effect was reversed by silencing the expression of the forkhead box protein O1 in the RAW264.7 macrophage hypoxia/reoxygenation model. In conclusion, our results suggest that LKB1 exerts a protective effect against liver IRI by downregulating the NLRP3 inflammasome., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The effect of different administration routes of omeprazole remains unclear on the recovery in patients with obesity after laparoscopic sleeve gastrectomy (LSG)., Methods: We designed a randomized clinical trial enrolling 120 patients with a BMI≥32.5 kg/m 2 after LSG. They were randomized into two groups to be administered with omeprazole by rapid intravenous injection (group A) or by continuous micropump infusion (group B). The plasma concentration of omeprazole was monitored upon initiating administration. Change in intragastric pH and gastrointestinal symptoms during follow-up served as indicators for therapeutic evaluation., Results: Patients in the two groups showed no difference in the AUC curves (P=0.25), but group A had significantly higher peak concentration (P<0.001), and shorter time to reach peak concentration after administration (P<0.001), compared to group B. Before and after the administration of omeprazole, the average change in intragastric pH was much lower in group A (0.031 ± 0.61) than in group B (0.48 ± 0.74) (P=0.004). The incidence of gastrointestinal symptoms was similar between the two groups (P=0.85); however, the average duration of remaining symptoms was longer in group A (3.97 months; 95% CI, 2.90-5.04) than in group B (2.82 months; 95% CI, 2.01-3.63) (P=0.04)., Conclusion: Continuous micropump infusion of omeprazole may improve the outcomes in patients with obesity after LSG., Trial Registration: China Clinical Trial Registration Center (ChiCTR), ChiCTR-IPR-17013365. Registered 13 November 2017. http://www.chictr.org.cn/showproj.aspx?proj=22892., Competing Interests: The authors declare that they have no competing interests., (© 2021 Tan et al.)

Water hyacinth (Eichhornia crassipes), a worst invasive aquatic weed has been caused the widespread problems for the water bodies and water resources, particularly the case in China. Plant pathogens are a promising alternative as biocontrol agents (Dagno et al. 2011), but success in this strategy will require the selection of some highly virulent pathogen strains. In September 2020, irregular necrotic lesions on leaves, stems, as well as crown and petiole rots symptoms, occurred on water hyacinth, in Minjiang and Xiyuanjiang watershed, in Fuzhou, China. Fragments from symptomatic leaf tissue (5x5mm) were superficially disinfected in 0.1% MgCl2 solution for 30 s, followed by rinsing three times in sterile water, placed on potato dextrose agar (PDA), and then incubated in darkness at 28°C for 5 days. Two fungal isolates (F3 and F11) were recovered and obtained pure cultures from the affected leaves and deposited in the Institute of Oceanography, Minjiang University. The colonies were stale, with felted, dense, pale grey aerial mycelium, scattered dark based acervuli with orange conidial masses near centre; in reverse side pinkish orange with patches of grey pigment near centre. The hyphae were septate, branched, and 2 to 6 µm in width. Appressoria were not observed. Conidiogenous cells were 20-24 × 3.5-4.5 µm, cylindric to flask-shaped, towards margin the conidiophores with a much looser structure, conidiogenous loci at apex and often also at septa. Asci were 60-80 × 15-20 µm, cylindric to subfusoid, 8-spored. Ascospores were 17-23 × 4-6 µm, gently curved, tapering to quite narrow, rounded ends. Perithecia mature after about 15 days, and were dark brown, subglobose, and 50-150 μm in diameter, and with scattered, dark brown setae about 50-80 µm long. Conidia were 15-25 × 4.5-6 μm, unicellular, colorless, and cylindrical to fusiform. Genomic DNA from two isolates was extracted with a modified DNA Midi Kit (TIANGEN, Inc., Beijing, China), and amplified using ITS4/ITS1F, CL1/CL2A, CHS-79F/CHS-345R, T1/T2 and GDF/GDR primers by PCR (Weir et al. 2012; White et al. 1990). Sequences of F3 and F11 were submitted to GenBank (accession no. ITS, MW307302, MW307303; CAL, MW303427, MW303429; CHS-1, MW303428, MW303430; TUB, MW531006, MW531007; GADPH, MW531008, MW531009). A phylogenetic tree using the maximum likelihood methods and including ITS-CHS-CAL-TUB-GADPH concatenated sequences from Colletotrichum gloeosporioides complex was obtained (Cai et al. 2009; Damm et al. 2018; Weir et al. 2012). Phylogenetic analyses revealed that isolate F3 and F11 were grouped into the clade C. fructicola. To test Koch's postulates, conidial suspensions (107 CFU/ml) of the isolate F3 and F11 were micro-injected into 20 water hyacinth seedlings per isolate. Another 20 seedlings were injected with water without conidia as control. Inoculated plants were kept in 50-liter plastic tanks, and maintained in a greenhouse at room temperature (19-24ºC) for two weeks. The Koch's test was conducted twice. After 10 days, typical anthracnose symptoms similar to the field appeared on the inoculated leaves, while the control leaves remained asymptomatic. The C. fructicola was re-isolated and identified by microscopy, PCR and sequencing, but not on non-inoculated controls. Anthracnose disease caused by C. fructicola has been reported affecting numerous plants worldwide, including cotton, coffea, grape, citrus, ect (Guarnaccia et al. 2017). However, to our knowledge, this is the first report of C. fructicola causing anthracnose on water hyacinth in China. Further studies for the efficacy of C. fructicola and/or of the genus Colletotrichum as biocontrol agent for water hyacinth or another aquatic plant are required (Ding et al. 2007; Dagno et al. 2012).

In 2019, transferable plasmid-borne tet (X3)/ tet (X4) genes conferring high-level tigecycline resistance were identified in Enterobacteriaceae and Acinetobacter . These transferable tet (X) variants are associated with different plasmids and could further spread and disseminate through associated mobile plasmids, raising public concern. In this study, we report the identification and characterization of two novel plasmids carrying tet (X4) in Escherichia coli isolated from retail chicken meat. We believe that our study contributes to our understanding of the genetic environment of tet (X4) and their transferability and capability of recombination and integration with other resistance genes in plasmids.

Lung cancer is the most common cause of cancer-related deaths worldwide. Pathologically, lung cancer can be non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC), while NSCLC accounts for approximately 85% of lung cancer patients. Stage III NSCLC represents a heterogeneous group of disease entities that are potentially curable and are usually dealt with multimodality treatments involving radiotherapy, chemotherapy, and surgical resection. Immune checkpoint inhibitors (ICIs) target programmed cell death receptor-1 (PD-1) and programmed death-ligand 1 (PD-L1). Studies have shown that ICIs have excellent and long-lasting anti-cancer effects in many cancers. The PACIFIC study is the first in the systemic treatment of stage III unresectable NSCLC in the past few decades that both progression-free survival (PFS) and overall survival (OS) have obtained positive results, However, the performance of this treatment strategy remains to be studied in a real-world setting. Such as who will benefit from treatment is still worthy of our continuous exp loration. In this paper, a patient with locally advanced unresectable NSCLC who underwent concurrent chemoradiotherapy followed by sequential immunotherapy (durvalumab) was reported. The patient obtained sustained clinical benefits despite low PD-L1 expression. This case report may serve as a reference for clinicians to make diagnostic and treatment decisions in clinical practice.

Plastid-encoded genes are coordinately transcribed by the nucleus-encoded RNA polymerase (NEP) and the plastid-encoded RNA polymerase (PEP). Resulting primary transcripts are frequently subject to RNA editing by cytidine-to-uridine conversions at specific sites. The physiological role of many editing events is largely unknown. Here, we have used the CRISPR/Cas9 technique in rice to knock out a member of the PLS-DYW subfamily of pentatricopeptide repeat (PPR) proteins. We found that OsPPR16 is responsible for a single editing event at position 545 in the chloroplast rpoB messenger RNA (mRNA), resulting in an amino acid change from serine to leucine in the β-subunit of the PEP. In striking contrast to loss-of-function mutations of the putative orthologue in Arabidopsis, which were reported to have no visible phenotype, knockout of OsPPR16 leads to impaired accumulation of RpoB, reduced expression of PEP-dependent genes, and a pale phenotype during early plant development. Thus, by editing the rpoB mRNA, OsPPR16 is required for faithful plastid transcription, which in turn is required for Chl synthesis and efficient chloroplast development. Our results provide new insights into the interconnection of the finely tuned regulatory mechanisms that operate at the transcriptional and post-transcriptional levels of plastid gene expression., (©2020 The Authors. New Phytologist ©2020 New Phytologist Foundation.)

Acute lung injury (ALI) is a life-threatening disorder with high rates of morbidity and mortality. Reactive oxygen species and epithelial apoptosis are involved in the pathogenesis of acute lung injury. Ferroptosis, an iron-dependent non-apoptotic form of cell death, mediates its effects in part by promoting the accumulation of reactive oxygen species. The inhibition of ferroptosis decreases clinical symptoms in experimental models of ischemia/reperfusion-induced renal failure and heart injury. This study investigated the roles of inhibitor of apoptosis-stimulating protein of p53 (iASPP) and Nrf2 in ferroptosis and their potential therapeutic effects in intestinal ischemia/reperfusion-induced acute lung injury. Intestinal ischemia/reperfusion-induced ALI was induced in wild-type and Nrf2 -/- mice. The mice were treated with erastin followed by liproxstatin-1. Ferroptosis-related factors in mice with ischemia/reperfusion-induced acute lung injury or in mouse lung epithelial-2 cells with hypoxia/regeneration (HR)-induced ALI were measured by western blotting, real-time PCR, and immunofluorescence. Ferroptosis contributed to intestinal ischemia/reperfusion-induced ALI in vivo. iASPP inhibited ferroptosis and alleviated intestinal ischemia/reperfusion-induced acute lung injury, and iASPP-mediated protection against ischemia/reperfusion-induced ALI was dependent on Nrf2 signaling. HR-induced acute lung injury enhanced ferroptosis in vitro in mouse lung epithelial-2 cells, and ferroptosis was modulated after the enhancement of intestinal ischemia/reperfusion in Nrf2 -/- mice. iASPP mediated its protective effects against acute lung injury through the Nrf2/HIF-1/TF signaling pathway. Ferroptosis contributes to intestinal ischemia/reperfusion-induced ALI, and iASPP treatment inhibits ferroptosis in part via Nrf2. These findings indicate the therapeutic potential of iASPP for treating ischemia/reperfusion-induced ALI.

This study aimed to analyze the relation between long noncoding RNA (lncRNA) LINCE00630 and radio-resistance and elucidate the underlying mechanism. Relative expression of LINC00630, BEX1, and DNMT3B in colorectal cancer (CRC) cells and clinical samples was determined by real-time PCR. Prognosis in respect of LINC00630 expression was analyzed by Kaplan-Meier survival curve. LINC00630 and BEX1 were specifically silenced by shRNAs. Cell viability and growth were analyzed by MTT and clonogenic assays, respectively. Cell apoptosis was measure by both caspase-3 activity and flow cytometry. Association between EZH2 with LINC00630 and BEX1 promoter was determined by RNA immunoprecipitation and chromatin immunoprecipitation. BEX1 and DNMT3B proteins were quantified by Western blot. We demonstrated the elevated LINC00630 correlated with radio-resistance and poorer prognosis in CRC. Knockdown of LINC00630 significantly improved the sensitivity of CRC cells to irradiation. Mechanistically, LINC00630 in complex with EZH2 negatively regulated BEX1 through promoter DNA methylation. BEX1 silencing greatly restored the cell viability and suppressed cell apoptosis, which were elicited by LINC00630 deficiency in response to irradiation. Our data uncovered the contribution of elevated LINC00630 to radio-resistance in CRC, which was predominately mediated by epigenetically repressed BEX1., (© 2020 International Union of Biochemistry and Molecular Biology.)

The quaternary chalcogenides consisting of earth-abundant elements such as Cu2ZnSnSe4 (CZTSe) have promising electrical and optical properties prompting enormous technological interest. Understanding different types of defects including Cu/Zn ordering is believed to be the key point to tackle technological challenges such as a large open circuit voltage deficit in CZTSe. The Te doped Cu2.2Zn0.8SnSe4-xTex (x = 0.01-0.04) were investigated using X-ray absorption fine structure spectroscopy at the Cu, Zn, and Se K-edges as well as at the Te L3-edge. Cu at the zinc site with anti-site defects and oxygen interstitials are identified. The detailed electronic structure upon Te doping is studied, providing insights into the rich defect chemistry present in this compound.

Esophageal squamous cell carcinoma (ESCC) is a predominant cancer type in developing countries such as China, where ESCC accounts for approximately 90% of esophageal malignancies. Lacking effective and targeted therapy contributes to the poor 5-year survival rate. Recent studies showed that about 30% of ESCC cases have high levels of SOX2. Herein, we aim to target this transcription factor with aptamer. We established a peptide aptamer library and then performed an unbiased screening to identify several peptide aptamers including P42 that can bind and inhibit SOX2 downstream target genes. We further found that P42 overexpression or incubation with a synthetic peptide 42 inhibited the proliferation, migration, and invasion of ESCC cells. Moreover, peptide 42 treatment inhibited the growth and metastasis of ESCC xenografts in mouse and zebrafish. Further analysis revealed that P42 overexpression led to alternations in the levels of proteins that are important for the proliferation and migration of ESCC cells. Taken together, our study identified the peptide 42 as a key inhibitor of SOX2 function, reducing the proliferation and migration of ESCC cells in vitro and in vivo, and thereby offering a potential therapy against ESCC., (Copyright © 2020 The American Society of Gene and Cell Therapy. Published by Elsevier Inc. All rights reserved.)

On the basis of phase-field theory, we develop a lattice Boltzmann model for ternary fluids containing solid. We develop a modified bounce-back method to describe the interactions between the solid and N-phase (N≥2) fluids. We derive a wetting boundary condition for three-phase flows from the point of mass conservation and propose a scheme for implementing the wetting condition on curved boundaries. We develop a diffuse interface method to compute the capillary force acting on the moving solid objects at the ternary fluids-sold contact lines. In addition, this model can deal with problems involving high density and viscosity contrasts. The proposed method is examined through several test cases. We test the modified bounce-back scheme, wetting boundary condition, and capillary force model in three different cases, and the numerical results agree well with the analytical solutions. Finally, we apply the model to two three-dimensional problems to assess its numerical accuracy and stability.

The interacting forces on the objects at the air-liquid interface are important for researching self-assembly of objects. Due to the interacting forces among objects, the objects self-assemble at the air-liquid interface and organize into ordered structures. In general, for the interacting of oil drops, they can attract coalescence or repel dispersion. However, according to our former research, we find that interactions of oil drops can be motion like interactions of gas atoms. The oil drops cannot coalesce to form a big oil drop or separate to form ordered structures. They attract at a long distance but repel when they almost contact. In this study, according to our simulation, we demonstrate that the atomic-like motion of oil drops is mainly caused by the surface tension gradient and the lateral capillary force. Based on the results, our research will facilitate the fundamental understanding about interactions among oil drops. Apart from giving detailed demonstration about the interacting forces among oil drops, our research may also put forward research about self-assembly, oil emulsification, and microfluidics.

Based on phase-field theory, we develop a lattice Boltzmann (LB) model for liquid-gas-solid flow from multiphase and particle dynamics algorithms. A modified bounce-back method is developed for the velocity-based LB approach. A curved boundary treatment with second-order accuracy based on velocity interpolation is developed. We propose a predictor-corrector scheme algorithm for specifying the three-phase contact angle on curved boundaries within the framework of structured Cartesian grids. In order to make the algorithm more stable, we combine the implicit particle velocity update scheme and the Galilean invariant momentum exchange method. The proposed method is validated through several single- and multicomponent fluid test cases. It was found the surface tension force associated with the interface acting on the solid structures can be captured. We simulate the sinking of a circular cylinder due to gravity, the numerical results agree well with the experimental data. Finally, we apply the method to the self-assembly process of multiple floating cylinders on water surface.

Drug-induced liver injury (DILI) is a major cause of acute liver failure (ALF) as a result of accumulated drugs in the human body metabolized into toxic agents and helps generate heavy oxidative stress, inflammation, and apoptosis, which induces necrosis in hepatocytes and ultimately damages the liver. Sirtuin 1 (SIRT1) is said to have multiple vital roles in cell proliferation, aging, and antistress systems of the human body. The levels of SIRT1 and its activation precisely modulate its critical role in the interaction between multiple step procedures of DILI. The nuclear factor kappa-light-chain-enhancer of activated B cell- (NF- κ B-) mediated inflammation signaling pathway, reactive oxygen species (ROS), DNA damage, mitochondrial membrane potential collapse, and endoplasmic reticulum (ER) stress also contribute to aggravate DILI. Apoptosis is regarded as the terminal reaction followed by multiple signaling cascades including caspases, p53, and mitochondrial dysfunction which have been said to contribute in DILI. The SIRT1 activator is regarded as a potential candidate for DILI, because the former could inhibit signaling of p53, NF- κ B, and ER stress. On the other hand, overexpression of SIRT1 also enhances the activation of antioxidant responses via Kelch-like ECH-associated protein 1- (Keap1-) nuclear factor- (erythroid-derived 2-) like 2 (Nrf2) signaling. The current manuscript will highlight the mechanism of DILI and the interaction of SIRT1 with various cytoplasmic factors leading to DILI along with the summary of potent SIRT1 agonists.

Wettability of artificial surfaces is attracting increasing attention for its relevant technological applications. Functional performance is often achieved by mimicking the topographical structures found in natural flora and fauna; however, surface attributes inspired by geological landscapes have so far escaped attention. We reproduced a stratified morphology of plateaus with a bi-Gaussian height distribution using a three-dimensional direct laser lithography. The plateau-inspired artificial surface exhibits a hydrophobic behavior even if fabricated from a hydrophilic material, giving rise to a new wetting mechanism that divides the well-known macroscopic Wenzel and Cassie states into four substates. We have also successfully applied the plateau-inspired structure to droplet manipulation.

Wetting mechanisms on rough surfaces were understood from either a monolayer or a multiscale perspective. However, it has recently been shown that the bi-Gaussian stratified nature of real surfaces should be accounted for when modeling mechanisms of lubrication, sealing, contact, friction, acoustic emission, and manufacture. In this work, a model combining Wenzel and Cassie theories was put forward to predict the static contact angle of a droplet on a bi-Gaussian stratified surface. The model was initially applied to numerically simulated surfaces and subsequently demonstrated on hydrophilic steel and hydrophobic self-assembled monolayer specimens with preset bi-Gaussian stratified topographies. In the Wenzel state, both the upper and the lower surface components are fully wetted. In the Cassie state, the upper component is still completely wetted, while the lower component serves as gas traps and reservoirs. By this model, wetting evolution was assessed, and the existence of different wetting states and potential state transitions was predicted.

Chaenomeles plants are adapted to diverse ecological zones particularly the temperate areas of Korea, Japan, and China. In China, Chaenomeles speciosa is mainly planted in Chongqing, Anhui, and Hubei provinces. Most of the studies till date have been focused on the anti-inflammatory activities of C. speciosa fractions. The present study aimed to review the maximum literature reported for the presence of various phytochemicals in C. speciosa . In addition, the pharmacological properties of these chemical compounds of this plant shall also be discussed. The extracts of the various parts of the plant are rich in diversity of antioxidants, organic acids, phenolics, terpenoids, and many different phytochemicals that bear strong anticancer, antioxidant, antiviral, antibacterial properties, anti-inflammation, antihyperlipidemic, antihyperglycemic, and anti-Parkinson properties. C. speciosa fruits have broad scope in industry as well as in medicines. Not only the leaves and fruits of C. speciosa plant, but various other parts including roots, seeds, bark twigs, and flowers all have long history of clinical trials in curing many human ailments. However, the maximum accessible data concerning the chemical compositions and their broad pharmacological properties of C. speciosa plant parts is pretty restricted that make it more appealing for in-depth investigations.

Background: Vancomycin is a first-line antibiotic used for the treatment of severe gram-positive bacterial infections. Clinical guidelines recommend that the vancomycin trough concentration be 10-15 mg/L for regular infections and 15-20 mg/L for severe infections. We investigated whether increasing the vancomycin concentration would result in better clinical outcomes with sustainable adverse effects (AEs) in the Chinese population., Methods: A prospective, open, multicenter clinical observational study was performed in patients with gram-positive bacterial infections from 13 teaching hospitals. Patients received vancomycin therapeutic drug monitoring. Clinical, microbiological, and laboratory data were collected., Results: In total, 510 patients were enrolled, and 470 were evaluable, of whom 370 were adults and 100 were children; 35.53% had methicillin-resistant Staphylococcus aureus infections (vancomycin 50% minimum inhibitory concentration [MIC50] = 1, 90% minimum inhibitory concentration [MIC90] = 1), and 23.19% had Enterococcus species infections (vancomycin MIC50 = 1, MIC90 = 2). The average trough concentration was 10.54 ± 8.08 mg/L in adults and 6.74 ± 8.93 mg/L in children. The infection was eradicated in 86.22% of adults and 96% of children. Thirty-six vancomycin-related nephrotoxicity cases were reported in the enrolled population. No severe AEs or deaths were related to vancomycin therapy. Logistic regression analysis showed that trough concentration had no relationship with clinical outcomes (adults P = .75, children P = .68) but was correlated with adult nephrotoxicity (P < .0001). Vancomycin trough concentration had an applicable cut point at 13 mg/L., Conclusions: Our study shows that vancomycin trough concentration has no statistical correlation with clinical outcomes, and is an indicator of nephrotoxicity in the observed population. We found no evidence that increasing vancomycin trough concentration to 15-20 mg/L can benefit Chinese patients with complicated infections., Clinical Trials Registration: ChiCTR-OPC-16007920.

Background: Our aims in this prospective study were to evaluate the correlations between pharmacokinetic/pharmacodynamic (PK/PD) indices and the clinical/microbiological efficacy of vancomycin and to identify an appropriate PK/PD target in the Chinese population to guide vancomycin treatment in the clinic., Methods: Adult patients from 11 hospitals in China with gram-positive infections who received vancomycin therapy for ≥5 days and who were under therapeutic drug monitoring (TDM) were enrolled in this study. A 1-compartment population PK model was established and validated. The correlations between PK/PD indices (Cmin, Cmax, 0-24 hour area under the curve (AUC0-24), and AUC0-24/minimum inhibitory concentration (MIC) and clinical outcomes (clinical efficacy and bacterial eradication) were evaluated., Results: In total, 402 adult Chinese patients were enrolled. Among them, 380 patients were evaluable for PK analysis, and 334 were evaluable for PK/PD analysis. In the final population PK model, creatinine clearance (CLCR) was the significant covariate on CL (typical value, 3.87 L/hour; between-subject variability (BSV), 12.5%), and age was the significant covariate on volume of distribution (V) (typical value, 45.1 L; BSV, 24.8%). The univariate analysis showed that Cmax, AUC0-24, and AUC0-24/MIC were significantly different or marginally significantly different (P values were 0.009, 0.0385, and 0.0509, respectively) between microbiological outcome groups with coagulase-negative Staphylococcus infections. However, there were no significant differences (P > .05) in the above PK parameters by multivariate logistic regression analysis, indicating there was no independently associated factor., Conclusions: No significant correlations were identified between PK/PD indices and the clinical or microbiological efficacy of vancomycin in Chinese patients. The necessity of vancomycin TDM based on trough concentration and the current treatment target of AUC0-24/MIC ≥400 need to be further evaluated and confirmed in additional prospective studies.

Background: To investigate hypoglycemic activity and elucidate the active composition of the fruit blueberry ( Vaccinium corymbosum )., Methods: Methanol extracts of blueberry (MEB) were separated using a D101 macroporous resin column to yield quinic acid derivative (Fr.1)- and flavonoid (Fr.2)-rich fractions. The effects of the blueberry extracts on mRNA expression of GLUT-2 (glucose transporter type 2) and PPARγ (peroxisome proliferator-activated receptor-γ), as well as on the activities of PPRE (peroxisome proliferator response element) and NF-κB were analyzed in LO2 normal liver cells. Real-time PCR was used to detect the expression of GLUT-2, PPARγ, TNF-α, IL-1β, and IL-6 mRNA. The PPRE and NF-κB activities were detected by a luciferase reporter assay. Western blotting was used to detect the levels of PPARγ, GLUT-2, and p65. The active compositions were isolated using various chromatography columns, and were analyzed by NMR., Results: mRNA and protein expression of GLUT-2 and PPARγ were significantly increased upon treatment with 400 μg/mL extracts of blueberry ( P <0.05). The PPRE activity was also significantly increased in a dose-dependent manner upon administration of MEB ( P <0.05). Furthermore, the NF-κB activity induced by lipopolysaccharides was inhibited by MEB ( P <0.05). No fraction separated from MEB exhibited PPRE activation or NF-κB inhibition activity. Blueberry extract may execute its hypoglycemic activity by stimulating expression of GLUT-2 and PPARγ, and by inhibiting the inflammatory pathway. Together, quinic acid derivatives and flavonoids may result in a synergistic effect. Fourteen phenolic acids, including eight flavonoids, four quinic acid derivatives, and two other phenolic acids, were isolated and identified, and caffeoylquinic acid derivatives and quercetin glycosides were found to be the major constituents of blueberry., Conclusion: Blueberry may have hypoglycemic activity that functions through synergistic effects with caffeoylquinic acid derivatives and quercetin glycosides., Competing Interests: Disclosure The authors declare no conflicts of interest in this work.

Objective: To investigate the in vivo inhibitory effects of sodium houttuyfonate (SH) on symptom pattern of Qi-deficiency in rats induced by infection of bacterial biofilm on rat respiratory tract., Methods: Symptom pattern is a term used in Traditional Chinese Medicine (TCM) to define a cluster of symptoms in a medical condition. Based on the pattern, TCM therapies are administered. The symptom pattern used in this study was lung-Qi deficiency pattern identified in rats, which was induced by nasal intubation drip of Pseudomonas aeruginosa (P. aeruginosa) (two strains) to form bacterial biofilm on airway combined with stimulation of cold and fatigue. We measured the variations of the symptoms of the pattern, weight, spleen and thymus index, blood gas, lung bronchial tissue pathology and cytokine of rat in different treatments and control groups., Results: The rats of SH-treatment groups had not showed typical symptoms comparing with model group in the early stage of infection. The weight, spleen and thymus index of the SH-treatment groups were significantly higher comparing with untreated model group. The SH-treatment groups also showed higher O(2) partial pressure and lower CO(2) partial pressure than model group. Furthermore, we found that the bronchopulmonary section of SH-treatment groups not showed typical pathogenic variation in model group. The comparison of cytokine concentration in different groups indicated that SH could prevent the over-production of cytokine to reduce the inflammation occurrence., Conclusion: In the early stage of airway infection by biofilm of P. aeruginosa, application of SH can prevent the occurrence of lung-Qi deficiency pattern.

Objective: To determine the safe space for hyaluronic acid(HA) injection through anatomy study of temporal layers., Methods: 6 fresh and 8 formaldehyde-fixed cadaver heads were dissected. The skin soft-tissue layers of temporal region were incised through the cranial coronal plane and elevated layer by layer. The morphological features of layers were observed and documented, as well as the relationship of the superficial temporal artery (STA),the temporal branch of facial nerve (TFN) and the middle temporal vein(MTV) with corresponding layers. Relevant neasurements of the superficial temporal fat pad (sTFD) were recorded. With reference of cardever dissection, temporal region injection with HA was carried out clinically to confirm the safety and effect., Results: In the temporal region, from surface to the temporal fossa, the layers are skin, subcutaneous tissue, superfiacial temporal fascia (STF),loose areolar tissue, superficial layer of deep temporal fascia(sDTF), sTFD, deep layer of deep temporal fascia (dDTF),deep temporal fat pad (dTFD) and temporalis. The temporal skin is tightly attached with the subcutaneous tissue. The STA runs within the subcutaneous tissue on the STF, whereas the TFN within the areolar tissue was just beneath the STF. The loose areolar tissue is a potential layer space. The DTF splits into two sheets of fascia at the line 1 cm above the upper orbital rim to envelope the sTFD, within which the MTV runs backward. The dTFD is the temporal extension of buccal fat pad. With reference of cadever dissection, the target space of temporal HA injection was beneath the temporalis for the area superior to the MTV, whereas within the sTFD for the area inferior to the MTV.67 cases were completed with good result and no complication., Conclusions: In the upper area of temporal region adjacent to the frontal border, the sub-temporalis space is the safety space for HA injection, while inferior to the middle temporal vein and near the zygoma, the superficial temporal fat pad is the target space for safe HA injection.

The increasing multidrug resistance of Pseudomonas aeruginosa has become a serious public-health problem. In the present study, the inhibitory activities of sodium houttuyfonate (SH) against biofilm formation and alginate production in a clinical strain of P. aeruginosa (AH16) were investigated in vitro using crystal violet dying and standard curve methods, respectively. The cellular morphology of P. aeruginosa treated with SH was observed using a scanning electron microscope. Furthermore, reverse transcription-quantitative polymerase chain reaction was used to identify differences in the expression levels of genes associated with alginate biosynthesis as a result of the SH treatment. The results indicated that SH significantly inhibited biofilm formation, and decreased the levels of the primary biofilm constituent, alginate, in P. aeruginosa AH16 at various stages of biofilm development. In addition, scanning electron microscopy observations demonstrated that SH markedly altered the cellular morphology and biofilm structure of P. aeruginosa . Furthermore, the results from the reverse transcription-quantitative polymerase chain reaction analysis indicated that SH inhibited biofilm formation by mitigating the expression of the algD and algR genes, which are associated with alginate biosynthesis. Therefore, the present study has provided novel insights into the potent effects and underlying mechanisms of SH-induced inhibition of biofilm formation in a clinical strain of P. aeruginosa .

A series of alluaudite Na2 Fe3-x Mnx (PO4 )3 microcompounds, which self-assembled from primary nanorods, were prepared successfully through a solvothermal method. As a promising candidate cathode for sodium-ion batteries, it is necessary to obtain a deeper understanding of the relationship between the structure and physicochemical properties of these materials. The local electronic and geometric environments were systematically investigated, for the first time, by using a combination of soft/hard X-ray absorption, IR, and Mössbauer spectroscopy. The results show that the electrochemical performance is not only associated with morphology, but also with the electronic and crystalline structure. With the introduction of manganese into the lattice, the long-range order maintains the isostructural framework and the lattice parameters expand as expected. However, for short-range order, PO4 tetrahedra and MO6 octahedra (M=Fe and Mn) become more severely distorted as a function of Mn concentration. Meanwhile, larger MnO6 octahedra will compress the space of FeO6 octahedra, which will result in stronger core/electron-electron interactions for Fe, as characterized by hard/soft X-ray absorption spectra. These slight changes in the electronic and local structures lead to different electrochemical performances with changes to the manganese content. Moreover, other physicochemical properties, such as magnetic behavior, are also confirmed to be correlated with these different electron interactions and local geometric environments., (© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Sodium houttuyfonate (SH) has been found to be mildly anti-pathogenetic against the planktonic and biofilm phenotypes of Pseudomonas aeruginosa. Here, we have attempted to investigate further the anti-pathogenicity of SH and EDTA-Na₂ in combination and in vitro and in vivo against planktonic and biofilm phenotypes of Pseudomonas aeruginosa (16 strains), Staphylococcus aureus (13 strains) and Candida albicans (13 strains). The antimicrobial activity of SH against all three pathogens increased dramatically when it was combined with EDTA-Na₂, in vitro. Toxic reactions to the drugs when administered orally were insignificant in mice; no abnormalities were observed in the internal organs, such as the lungs and kidneys. Finally, the results of in vivo studies indicate that SH could extend the lifespan of infected animals when administered in combination with EDTA-Na2. Therefore, the results of the present study lead us to suggest that SH could be a promising antimicrobial agent and that SH combined with EDTA-Na₂ has the potential to be an excellent choice of drug for combating bacterial infections clinically.

The mechanism for the decreasing critical temperature (T(C)) of the metal-insulator transition (MIT) in vanadium dioxide (VO2) by tungsten (W) doping is a matter of debate. Here, to clarify the correlation between W doping and T(C), the electronic and geometrical structures around W and V atoms in W(x)V(1-x)O2 samples are systematically investigated by X-ray absorption fine structure (XAFS) spectroscopy. The evidence of electron doping of W(6+) ions in VO2 is obtained from the reduction of V(4+) to V(3+) ions. This kind of electron doping has been considered to favor the MIT process. Moreover, from the XAFS results, the local rutile structure around W dopants is identified even at low doping, and acts as the structure-guided domain to facilitate the MIT in VO2. Considering the electronic band structures of W(x)V(1-x)O2 samples, the internal stresses induced by W(6+) doping yield the detwisting of the nearby monoclinic VO2 lattice. This lattice detwisting will drive the downward shift of the π* electron band and a smaller separation between antibonding and bonding d∥ orbitals in the band structure of VO2, which induces the decreased band gaps of W(x)V(1-x)O2 samples. As a consequence, the potential energy barrier for phase transition is lowered and the reduced T(C) is observed.

The heat shock proteins (Hsps) play a positive role in lifespan determination, and histone acetylation has been shown to be involved in transcription of hsp genes in Drosophila. To further determine if hsp22 and hsp70 expression is correlated with lifespan, and if histone acetylation participates in this process, RNA levels for hsp22 and hsp70 were analyzed throughout the lifespan in the long-lived and short-lived iso-female lines. The results showed that hsp22 and hsp70 RNA levels were higher in long-lived line than in short-lived line and that the long-lived flies responded more rapidly to heat but were more tolerant to high temperature. Moreover, we investigated the influences of histone acetylation modification on longevity and on hsp gene expression by using histone deacetylase (HDAC) inhibitors TSA and BuA. The results demonstrated that both inhibitors were able to extend the lifespan and promote hsp22 and hsp70 expression. However, the optimal concentrations of these inhibitors, and probably the mechanisms of their actions, vary with the genetic background. In addition, we showed that HDAC inhibitors caused the hyperacetylation of core histone H3, implicating the involvement of chromatin modulation in hsp gene transcription. These data suggested a close correlation among histone acetylation, hsp gene expression and longevity in D. melanogaster.