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The carbon–carbon triple bond (–C≡C–) is an elementary constituent for the construction of conjugated molecular wires and carbon allotropes such as carbyne and graphyne. Here we describe a general approach to in situ synthesize –C≡C– bond on Cu(111) surface via homo-coupling of the trichloromethyl groups, enabling the fabrication of individual and arrays of poly( p -phenylene ethynylene) molecular wires. Scanning tunneling spectroscopy reveals a delocalized electronic state extending along these molecular wires, whose structure is unraveled by atomically resolved images of scanning tunneling microscopy and noncontact atomic force microscopy. Combined with density functional theory calculations, we identify the intermediates formed in the sequential dechlorination process, including surface-bound benzyl, carbene, and carbyne radicals. Our method overcomes the limitation of previous on-surface syntheses of –C≡C– incorporated systems, which require the precursors containing alkyne group; it therefore allows for a more flexible design and fabrication of molecular architectures with tailored properties. Incorporating carbon-carbon triple bonds into conjugated chains typically requires acetylenic precursors. Here, the authors synthesize poly( p -phenylene ethynylene) molecular wires on Cu(111) by directly coupling trichloromethyl-containing precursors, forming C-C triple bonds in situ

Background： Trichophyton rubrum is superficial fungi characteristically confined to dead keratinized tissues. These observations suggest that the soluble components released by the fungus could influence the host immune response in a cell in contact-free manner. Therefore, this research aimed to analyze whether the culture supernatant derived from T. rubrum grown in the nail medium could elicit the immune response of keratinocyte effectively. Methods： The culture supernatants of two strains （T1a, TXHB） were compared for the β-glucan concentrations and their capacity to impact the innate immunity of keratinocytes. The β-glucan concentrations in the supernatants were determined with the fungal G-test kit and protein concentrations with bicinchoninic acid protein quantitative method, then HaCaT was stimulated with different concentrations of culture supernatants by adopting morphological method to select a suitable dosage. Expressions of host defense genes were assessed by quantitative polymerase chain reaction after the HaCaT was stimulated with the culture supernatants. Data were analyzed with one-way analysis of variance, followed by the least significant difference test. Results： The T. rubrum strains （T1a and TXHB） released β-glucan of 87.530 ± 37.581 pg/ml and 15.747 ± 6.453 pg/ml, respectively into the media. The messenger RNA （mRNA） expressions of toll-like receptor-2 （TLR2）, TLR4, and CARD9 were moderately up-regulated in HaCaT within 6-h applications of both supernatants. HaCaT cells were more responsive to Tla than TXHB. The slight increase of dendritic cells-specific intercellular adhesion molecule 3-grabbing nonintegrin expression was faster and stronger, induced by T1a supematant than TXHB. The moderate decreases of RNase 7, the slight up-regulations of Dectin-1 and interleukin-8 at the mRNA level were detected only in response to T la rather than TXHB After a long-time contact, all the elevated defense genes decreased alter 24 h. Conclusion： The culture supernatant of T. rubrum could directly and transiently activate the innate immune response of keratinocytes.

Aim： To investigate the effects of deferiprone on doxorubicin-induced cardiotoxicity and determine its protection on cardiac contractility in vivo at tissue level. Methods： Spontaneously-beating isolated atria from rats were pretreated with deferiprone for 10 min at 1.2 mmol/L or 0.3 mmol/L, respectively before co-incubation with doxorubicin （DOX） at 0.03 mmol/L for 60 min. Contractility （dF/dt） was assessed every 10 min during the incubation. After that, the tissues around the sinuatrial nodes were fixed for ultrastructural study; succinate dehydrogenase （SDH） and Cu, Zn superoxide dismutase （Cu, Zn-SOD） activity, as well as malondialdehyde （MDA） level of the atria were assayed. Results： Treatment with DOX alone resulted in a 49.34% reduction of the contractility, mitochondria swelling, disruption of mitochondrial crista and decreased electron density of the matrices. Conversely, with the presence of deferiprone, the negative inotropic effect and lesions in the cardiac mitochondria structure induced by DOX were attenuated. Cu, Zn-SOD activity increased by 12.97%-12.11%, the MDA level decreased by 29.12%-39.82% and succinate dehydrogenase （SDH） activity was ameliorated by 25.15%-34.76%. Conclusion ： Deferiprone can efficiently preserve cardiac contractility. Moreover, the results of this study indicate that deferiprone is able to protect mitochondrial function and structure form damage induced by DOX. This cardiac protective potential of deferiprone could be due to its defense capability against oxidative damage.

Background：To compare the diagnostic values of magnetic resonance elastography （MRE） and diffusion-weighted imaging （DWI） in staging hepatic fibrosis （HF） in an animal model.Methods：This study consisted of 44 rabbits served as HF group and 9 normal rabbits.HF group was divided into two subgroups：Group A （n =32） and Group B （n =12）.Rabbits in Group B were served as a complementary group when rabbits in Group A suddenly died during the study.Rabbits from control and Group A underwent abdominal MR imaging （MRI）,MRE,and DWI.In Group A,random eight rabbits underwent MRI examinations at 4,5,6,l0 weeks after carbon tetrachloride oil subcutaneous injection.Liver stiffness （LS） and apparent diffusion coefficient （ADC） values of liver parenchyma were measured.The diagnostic performance of MRE and DWI for staging HF was compared using the receiver operating characteristic curve analysis on the basis of the histopathological analysis of HF.Results：Significant differences of LS and DWI values were present among HF stages （P 〈 0.005）.The LS values measured on MRE （r =0.838,P 〈 0.001） were more strongly correlated with the HF stages than with ADC values （r =-0.527,P 〈 0.001）.The area under the receiver operating characteristic curve values of LS were significantly larger than those of DWI were for discriminating two stages of HF （0.979 vs.0.712 for ≥ S 1,0.922 vs.0.699 for ≥ S2）.MRE showed higher specificity for predicting all stages of HF compared to DWI.Conclusions：MRE more strongly correlated with the HF stages than DWI and is more specific in predicting all HF stages.

Background： Trichophyton rubrum represents the most common infectious fungus responsible for dermatophytosis in human, but the mechanism involved is still not completely understood. An appropriate model constructed to simulate host infection is the prerequisite to study the pathogenesis of dernlatophytosis caused by T.. rubrum. In this study, we intended to develop a new T. rubrum infection model in vitro, using the three-dimensional reconstructed epidermis - EpiSkin, and to pave the way for further investigation of the mechanisms involved in T. rubrum infection. Methods： The reconstructed human epidermis （RHE） was infected by inoculating low-dose （400 conidia） and high-dose （4000 conidia） T. rubrum conidia to optimize the infection dose. During the various periods after infection, the samples were processed for pathological examination and scanning electron microscopy （SEM） observation. Results： The histological analysis of RHE revealed a fully differentiated epidermis with a functional stratum corneum, which was analogous to the normal human epidermis. The results of hematoxylin and eosin staining and the periodic acid-Schiff staining showed that the infection dose of 400 conidia was in accord with the pathological characteristics of host dermatophytosis caused by T. rubrum. SEM observations further exhibited the process of 77 ruhrum infection in an intuitionistic way, Conclusions： We established the T. rubrum infection model on RHE in vitro successfully. It is a promising model fbr further investigation of the mechanisms involved in T. rubrum infection.

Key-value （KV） stores have become a backbone of large-scale applications in today＇s data centers. Write- optimized data structures like the Log-Structured Merge-tree （LSM-tree） and their variants are widely used in KV storage systems like BigTable and RocksDB. Conventional LSM-tree organizes KV items into multiple, successively larger components, and uses compaction to push KV items from one smaller component to another adjacent larger component until the KV items reach the largest component. Unfortunately, current compaction scheme incurs significant write amplification due to repeated KV item reads and writes, and then results in poor throughput. We propose a new compaction scheme, delayed compaction （dCompaction） that decreases write amplification, dCompaction postpones some compactions and gathers them into the following compaction. In this way, it avoids KV item reads and writes during compaction, and consequently improves the throughput of LSM-tree based KV stores. We implement dCompaction on RocksDB, and conduct extensive experiments. Validation using YCSB framework shows that compared with RocksDB, dCompaction has about 40% write performance improvements and also comparable read performance.

This paper derives the bounded real lemmas corresponding to L∞ norm and H∞ norm (L-BR and H-BR) of fractional order systems. The lemmas reduce the original computations of norms into linear matrix inequality (LMI) problems, which can be performed in a computationally efficient fashion. This convex relaxation is enlightened from the generalized Kalman-Yakubovich-Popov (KYP) lemma and brings no conservatism to the L-BR. Meanwhile, an H-BR is developed similarly but with some conservatism. However, it can test the system stability automatically in addition to the norm computation, which is of fundamental importance for system analysis. From this advantage, we further address the synthesis problem of H∞ control for fractional order systems in the form of LMI. Three illustrative examples are given to show the effectiveness of our methods.

Neonicotinoid insecticides, which target insect nicotinic acetylcholine receptors (nAChRs), have been widely and intensively used to control the whitefly, Bemisia tabaci , a highly damaging, globally distributed, crop pest. This has inevitably led to the emergence of populations with resistance to neonicotinoids. However, to date, there have been no reports of target-site resistance involving mutation of B . tabaci nAChR genes. Here we characterize the nAChR subunit gene family of B . tabaci and identify dual mutations (A58T&R79E) in one of these genes ( BTβ1 ) that confer resistance to multiple neonicotinoids. Transgenic D . melanogaster , where the native nAChR Dβ1 was replaced with BTβ1 A58T&R79E , were significantly more resistant to neonicotinoids than flies where Dβ1 were replaced with the wildtype BTβ1 sequence, demonstrating the causal role of the mutations in resistance. The two mutations identified in this study replace two amino acids that are highly conserved in >200 insect species. Three-dimensional modelling suggests a molecular mechanism for this resistance, whereby A58T forms a hydrogen bond with the R79E side chain, which positions its negatively-charged carboxylate group to electrostatically repulse a neonicotinoid at the orthosteric site. Together these findings describe the first case of target-site resistance to neonicotinoids in B . tabaci and provide insight into the molecular determinants of neonicotinoid binding and selectivity.

Breast cancer stem cells (BCSCs) play an essential role in facilitating breast cancer relapse and metastasis. The underlying mechanism, however, remains incompletely understood. In the current study, we investigated the clinical significance, biological function and mechanism of a long noncoding RNA CCAT1 (LncCCAT1) in BCSCs. Firstly, lncRNAs expression in poorly differentiated breast cancer tissues and BCSCs were measured by lncRNA microarray and confirmed in breast cancer tissues and cell lines. The functional roles and mechanisms of LncCCAT1 were further investigated by gain and loss of function assays and . LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. Mechanistic investigation suggests that LncCCAT1 can interact with miR-204/211, miR-148a/152 and Annexin A2(ANXA2), then upregulate T-cell factor 4 (TCF4) or promote translocation of β-catenin to the nucleus where it activates TCF4, leading to the activation of wingless/integrated (Wnt) signaling. Furthermore, TCF4 can also bind to the promoter of LncCCAT1 to promote LncCCAT1 transcription, thus forming a positive feedback regulatory circuit of LncCCAT1-TCF4-LncCCAT1 in BCSCs. LncCCAT1 plays an important role in breast cancer progression and may serve as a novel target for breast cancer diagnosis and therapy.

Breast cancer, the most prevalent cancer type among women worldwide, remains incurable once metastatic. Long noncoding RNA (lncRNA) and microRNA (miRNA) play important roles in breast cancer by regulating specific genes or proteins. In this study, we found miR-133b was silenced in breast cancer cell lines and in breast cancer tissues, which predicted poor prognosis in breast cancer patients. We also confirmed that lncRNA NEAT1 was up-regulated in breast cancer and inhibited the expression of miR-133b, and identified the mitochondrial protein translocase of inner mitochondrial membrane 17 homolog A (TIMM17A) that serves as the target of miR-133b. Both miR-133b knockdown and TIMM17A overexpression in breast cancer cells promoted cell migration and invasion both in vitro and in vivo. In summary, our findings reveal that miR-133b plays a critical role in breast cancer cell metastasis by targeting TIMM17A. These findings may provide new insights into novel molecular therapeutic targets for breast cancer.