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Geometric phase, associated with holonomy transformation in quantum state space, is an important quantum-mechanical effect. Besides fundamental interest, this effect has practical applications, among which geometric quantum computation is a paradigm, where quantum logic operations are realized through geometric phase manipulation that has some intrinsic noise-resilient advantages and may enable simplified implementation of multi-qubit gates compared to the dynamical approach. Here we report observation of a continuous-variable geometric phase and demonstrate a quantum gate protocol based on this phase in a superconducting circuit, where five qubits are controllably coupled to a resonator. Our geometric approach allows for one-step implementation of n -qubit controlled-phase gates, which represents a remarkable advantage compared to gate decomposition methods, where the number of required steps dramatically increases with n . Following this approach, we realize these gates with n up to 4, verifying the high efficiency of this geometric manipulation for quantum computation. Geometric phase is of fundamental interest and has practical application in quantum computation. Here the authors observe continuous-variable geometric phase in a superconducting circuit and demonstrate a multi-qubit controlled phase gate protocol based on this geometric effect.

Asiatic acid (AA) has been shown to induce apoptotic death in a range of cancers, but the mechanisms whereby it can inhibit tongue cancer growth have yet to be clarified. Herein, we explored the effects of AA on tongue cancer cells and found that it induced their apoptotic death in vitro and in vivo, while additionally impairing xenograft tumor growth in vivo. From a mechanistic perspective, AA treatment was associated with increases in levels of calcium and the calcium- dependent protease calpain, and it further induced endoplasmic reticulum (ER) stress and consequent Grp78-related IRE1α and JNK phosphorylation, ultimately driving caspase-3 activation and apoptotic death. Together, these results highlight AA as a promising tool for the therapeutic treatment of tongue cancer in clinical practice.

Background Coxsackievirus B3 (CV-B3) is usually associated with aseptic meningitis and myocarditis; however, the association between CV-B3 and hand, foot, and mouth disease (HFMD) has not been clearly demonstrated, and the phylogenetic dynamics and transmission history of CV-B3 have not been well summarized. Method Two HFMD outbreaks caused by CV-B3 were described in Hebei Province in 2012 and in Shandong Province in 2016 in China. To analyze the epidemiological features of two CV-B3 outbreaks, a retrospective analysis was conducted. All clinical specimens from CV-B3 outbreaks were collected and disposed according to the standard procedures supported by the WHO Global Poliovirus Specialized Laboratory. EV genotyping and phylogenetic analysis were performed to illustrate the genetic characteristics of CV-B3 in China and worldwide. Results Two transmissible lineages (lineage 2 and 3) were observed in Northern China, which acted as an important “reservoir” for the transmission of CV-B3. Sporadic exporting and importing of cases were observed in almost all regions. In addition, the global sequences of CV-B3 showed a tendency of geographic-specific clustering, indicating that geographic-driven adaptation plays a major role in the diversification and evolution of CV-B3. Conclusions Overall, our study indicated that CV-B3 is a causative agent of HFMD outbreak and revealed the phylogenetic dynamics of CV-B3 worldwide, as well as provided an insight on CV-B3 outbreaks for effective intervention and countermeasures.

The engineering of quantum devices has reached the stage where we now have small-scale quantum processors containing multiple interacting qubits within them. Simple quantum circuits have been demonstrated and scaling up to larger numbers is underway. However, as the number of qubits in these processors increases, it becomes challenging to implement switchable or tunable coherent coupling among them. The typical approach has been to detune each qubit from others or the quantum bus it connected to, but as the number of qubits increases this becomes problematic to achieve in practice due to frequency crowding issues. Here, we demonstrate that by applying a fast longitudinal control field to the target qubit, we can turn off its couplings to other qubits or buses. This has important implications in superconducting circuits as it means we can keep the qubits at their optimal points, where the coherence properties are greatest, during coupling/decoupling process. Our approach suggests another way to control coupling among qubits and data buses that can be naturally scaled up to large quantum processors.

The subgenotype B5 of EV-A71 is a widely circulating subgenotype that frequently spreads across the globe. Several outbreaks have occurred in nations, such as Malaysia, Thailand, Vietnam, and Japan. Appearing first in Taiwan, China, the subgenotype has been frequently reported in mainland of China even though no outbreaks have been reported so far. The current study reconstructed the migration of the B5 subgenotype of EV-A71 in China via phylogeographical analysis. Furthermore, we investigated its population dynamics in order to draw more credible inferences. Following a dataset cleanup of B5 subgenotype of EV-A71, we detected earlier B5 subgenotypes of EV-A71 sequences that had been circulating in Malaysia and Singapore since the year 2000, which was before the 2003 outbreak that occurred in Sarawak. The Bayesian inference indicated that the most recent common ancestor of B5 subgenotype EV-A71 appeared in September, 1994 (1994.75). With respect to the overall prevalence, geographical reconstruction revealed that the B5 subgenotype EV-A71 originated singly from single-source cluster and subsequently developed several active lineages. Based on a large amount of data that was accumulated, we conclude that the appearance of the B5 subgenotype of EV-A71 in mainland of China was mainly due to multiple migrations from different origins.

Enterovirus A90 (EV-A90) is a novel serotype of enterovirus A species that is rarely reported. Here, we isolated five enteroviruses from patients with acute flaccid paralysis in Hotan and Kashgar cities in Xinjiang, China that were identified as EV-A90 by molecular typing. The VP1 sequences of these Xinjiang EV-A90 strains showed 88.4–89% nucleotide sequence identity to the prototype EV-A90 strain; however, genome analysis indicated complex recombination events in P2 and P 3 regions. Next, the seroprevalence of EV-A90 was examined in 49 serum specimens collected in Hotan and Kashgar, and 37.5% were EV-A90 antibody positive (>1:8), with a geometric mean titre (GMT) of 1:10.47. The low positive rate and GMT suggest a low-level EV-A90 epidemic in Xinjiang. Two of the five Xinjiang EV-A90 strains were temperature sensitive, and three were temperature resistant, and a comparative genomics analysis suggested that an amino acid substitution (H1799Y) in the 3D pol region was related to temperature sensitivity. Although the epidemic strength is low, some EV-A90 strains were temperature resistant, which is suggestive of strong virulence and transmission capacity. This study expanded the number of EV-A90 in GenBank and provided basic data that may be useful for studying the molecular epidemiology of EV-A90.

Enterovirus B80 (EV-B80) is a newly identified serotype belonging to the enterovirus B species. To date, only two full-length genomic sequences of EV-B80 are available in GenBank, and few studies on EV-B80 have been conducted in China or worldwide. More information and research on EV-B80 is needed to assess its genetic characteristics, phylogenetic relationships, and association with enteroviral diseases. In this study, we report the phylogenetic characteristics of three Xinjiang EV-B80 strains and one Tibet EV-B80 strain in China. The full-length genomic sequences of four strains show 78.8-79% nucleotide identity and 94-94.2% amino acid identity with the prototype of EV-B80, indicating a tendency for evolution. Based on a maximum likelihood phylogenetic tree based on the entire VP1 region, three genotypes (A-C) were defined, revealing the possible origin of EV-B80 strains in the mainland of China. Recombination analysis revealed intraspecies recombinations in all four EV-B80 strains in nonstructural regions along with two recombination patterns. Due to the geographic factor, the coevolution of EV-B strains formed two different patterns of circulation. An antibody seroprevalence study against EV-B80 in two Xinjiang prefectures also showed that EV-B80 strains were widely prevalent in Xinjiang, China, compared to other studies on EV-B106 and EV-B89. All four EV-B80 strains are not temperature sensitive, showing a higher transmissibility in the population. In summary, this study reports the full-length genomic sequences of EV-B80 and provides valuable information on global EV-B80 molecular epidemiology.

Amaranthus retroflexus L. is one of the malignant weeds which can cause a reduction in the soybean yield. We found a population of A . retroflexus (R-Q) resistant to fomesafen through the initial screening of whole-plant dose response bioassay in the research. The resistance index of the population (R-Q) was 183 times of the sensitive population (S-N). The resistant and sensitive populations were used as experimental materials in the paper. Strand-specific RNA-Seq analyses of R‒Q and S‒N populations obtained from herbicide-treated and mock-treated leaf samples after treatment were conducted to generate a full-length transcriptome database. We analyzed differentially expressed genes (DEGs) among the R-Q and S‒N A . retroflexus populations treated with recommended dose and mock-treated on the 1 st (24 h) and 3 rd (72 h) days to identify genes involved in fomesafen resistance. All 82,287 unigenes were annotated by Blastx search with E-value < 0.00001 from 7 databases. A total of 94,815 DEGs among the three group comparisons were identified. Two nuclear genes encoding PPO ( PPX1 and PPX2 ) and five unigenes belonging to the AP2-EREBP, GRAS, NAC, bHLH and bZIP families exhibited different expression patterns between individuals of S‒N and R-Q populations. The A . retroflexus transcriptome and specific transcription factor families which can respond to fomesafen in resistant and susceptible genotypes were reported in this paper. The PPX1 and PPX2 genes of the target enzyme were identified. The study establishes the foundation for future research and provides opportunities to manage resistant weeds better.

Erlotinib is a commonly used molecular-targeted drug for the treatment of tongue cancer. However, the development of acquired resistance to erlotinib hampers its therapeutic use. To analyze the erlotinib resistance, long-term and short term survival assay were used to compare the resistance between parental and resistant tongue cancer cells. Flow cytometry, Hochest staining and western blot were used to analyze the apoptosis among the cells. Moreover, Transwell and wound healing assay were used to compare the invasion ability of the cells. To deeply explore the drug resistance in vivo, orthotopic tumor studies were applied. Finally, to explain the mechanism of c-met in erlotinib resistance, shRNA against c-met was used to down-regulate the expression of c-met. And SU11274 also used in orthotopic model. We established erlotinib-resistant human tongue cancer cell line by chronic exposure of TCA-8113 cells to increasing concentrations of erlotinib and determined the role of c-MET and EGFR in the development of acquired resistance. We found a significant increase in the phosphorylation of c-MET and an obvious decrease of the phosphorylation of EGFR in erlotinib-resistant cells. Our results also revealed that inhibition of c-MET alone with SU11274 exerted an inhibitory effect on the proliferation of erlotinib-resistant cells in the short term; however, it failed to sustain the inhibitory effect in the long term. Simultaneous inhibition of c-MET and EGFR significantly inhibited the proliferation of erlotinib-resistant cells in both a short and long period. Furthermore, we explored the underlying mechanism and found that treatment of erlotinib-resistant cells with SU11274 or shRNA against c-MET induced the phosphorylation of EGFR. Moreover, our results demonstrated that simultaneous inhibition of c-MET and EGFR significantly inhibited the migration and invasion of erlotinib-resistant cells. Taken together, our results suggested that c-MET is involved in acquired drug resistance to erlotinib and that cotargeting of EGFR and c-MET could overcome acquired resistance to erlotinib and inhibit the invasion and metastasis of erlotinib-resistant cells.

Tongue cancer originating on the surface of the tongue is most commonly squamous cell carcinoma, which has a higher invasive ability and a lower survival rate compared with other forms of tongue cancer. Notably, tongue squamous cell carcinomas metastasize into lymph nodes at early stages. Focal adhesion kinase (FAK) is an important protein tyrosine kinase involved in invasion and metastasis of cancer cells. In the present study, the role of FAK in the invasion and metastasis of tongue cancer was evaluated and the underlying mechanisms involved in this process were explored. FAK knockdown was performed using shRNA in the tongue cancer cell line, Tca-8113, and the invasion and metastasis potentials were analyzed using wound healing and transwell assays, respectively. Cytoskeletal arrangement was detected by fluorescence using TRITC-conjugated phalloidin staining. The activity of matrix metalloproteinase (MMP)-2 and -9 was examined by gelatin zymography. Paxillin distribution was observed by immunofluorescence. The levels of E-cadherin, N-cadherin, MMP-2 and -9, and c-Jun N-terminal kinase (JNK) was detected by western blot analysis. Wound healing and transwell assays demonstrated that FAK knockdown inhibited the invasion and metastasis of Tca-8113 cells. Further analysis revealed that FAK knockdown caused the rearrangement of the cytoskeleton and decreased the activity of MMP-2 and -9. Immunofluorescence analysis revealed that downregulation of FAK induced the relocalization of paxillin. Paxillin accumulated as dots and patches at the cell membrane in control cells. By contrast, in FAK knockdown cells, paxillin was distributed homogeneously in the cytoplasm. Western blot analysis revealed that FAK knockdown inhibited epithelial-mesenchymal transition (EMT) and decreased levels of MMP-2 and -9, and p-JNK. Knockdown of FAK inhibits the invasion and metastasis of Tca-8113 by decreasing MMP-2 and -9 activities and led to the rearrangement of the cytoskeleton and inhibited the EMT.