Experimental Realization of Robust Geometric Quantum Gates with Solid-State Spins.

We experimentally realize a universal set of single-bit and two-bit geometric quantum gates by adiabatically controlling solid-state spins in a diamond defect. Compared with the nonadiabatic approach, the adiabatic scheme for geometric quantum computation offers a unique advantage of inherent robustness to parameter variations, which is explicitly demonstrated in our experiment by showing that the single-bit gates remain unchanged when the driving field amplitude varies by a factor of 2 or the detuning fluctuates in a range comparable to the inverse of the gate time. The reported adiabatic control technique and its convenient implementation offer a paradigm for achieving quantum computation through robust geometric quantum gates, which is important for quantum information systems with parameter-fluctuation noise such as those from the inhomogeneous coupling or the spectral diffusion.

Novel SLCO2A1compound heterozygous mutation causing primary hypertrophic osteoarthropathy with Bartter-like hypokalemia in a Chinese family.

PURPOSE: Primary hypertrophic osteoarthropathy (PHO) is an inherited disease characterized by digital clubbing, periostosis and pachydermia with defects in the degradation of prostaglandin E2 (PGE2). Mutations in SLCO2A1 gene-encoding prostaglandin transporter (PGT) resulted in PHO, autosomal recessive 2 (PHOAR2). The spectrum of mutations and variable clinical complications of PHOAR2 has been delineated. In this study, we investigated a Chinese PHO family with a manifestation of Bartter-like hypokalemia. METHODS: Clinical manifestations were collected and genetic analyses were performed in the PHO family. RESULTS: The 33-year-old male proband had severe hypokalemia due to potassium loss from the kidney, while his brother had mild hypokalemia. After being treated with etoricoxib, the serum potassium level of the patient increased rapidly to the normal range which corresponded with the reduction in his serum PGE2 and PE2 metabolite (PGEM) levels. A novel SLCO2A1 compound heterozygous mutation of p.I284V and p.C459R was identified in two PHO patients in this family. CONCLUSIONS: The present findings supported that the Bartter-like hypokalemia is a new complication of PHOAR2 caused by the high level of PGE2. Etoricoxib was demonstrated to be effective for the renal hypokalemia in PHO patients.

Tuberculosis-associated mortality and its risk factors in a district of Shanghai, China: a retrospective cohort study.

SETTING: Pulmonary tuberculosis (PTB) causes a considerable number of deaths in China; however, the factors related to mortality are not well known. OBJECTIVE: To determine mortality among PTB patients and to explore its risk factors in Shanghai, China. DESIGN: This was a retrospective population-based study. A cohort of PTB patients who initiated treatment in a district of Shanghai from 2004 to 2015 was evaluated. Mortality in PTB patients was studied using the standardised mortality ratio (SMR) and Cox's proportional hazards model. RESULTS: Of 2741 PTB patients recruited in our study, 394 (14.4%) died during the 12-year follow-up. The summarised SMR was 2.8, and death was most likely to occur during the first months of anti-tuberculosis treatment. Age 60 years (adjusted hazard ratio [aHR] 4.039, P < 0.001), male sex (aHR 1.603, P < 0.001), sputum smear test positivity (aHR 1.945, P < 0.001), multidrug-resistant TB (MDR-TB; aHR 3.502, P = 0.001), diabetes mellitus (aHR 1.422, P = 0.012), chronic obstructive pulmonary disease (aHR 2.505, P < 0.001) and having cancer (aHR 4.319, P < 0.001) were risk factors for PTB mortality. CONCLUSION: The overall mortality in PTB patients was higher than that in the general population. MDR-TB and comorbidity were the two leading risk factors for mortality in PTB patients. Early, accurate diagnosis, together with comprehensive management and treatment, can reduce the mortality rate in PTB patients.

Correlation analysis of MR/CT on colorectal cancer lymph node metastasis characteristics and prognosis.

OBJECTIVE: Colorectal cancer incidence showed increasing trend with living standard improvement and lifestyle changes. This study investigated the relationship and diagnostic value of colorectal cancer lymph node metastasis and prognosis using magnetic resonance (MR) and computed tomography (CT). PATIENTS AND METHODS: Siemens Avanto 3.0T MR and GE Light Speed Pro 64 row helical CT were used to scan 318 cases of colorectal cancer patients diagnosed by pathology. The relationship between colorectal cancer lymph node metastasis and prognosis after surgery was analyzed. RESULTS: The accuracy of MR and CT in judging colorectal cancer lymph node metastasis ratio (LNR) was 92.5% and 75.5%, respectively. MR showed significantly higher accuracy than CT (p < 0.05). The coincidence rate of LNR result derived from MR and CT with colorectal cancer histopathological results was 57.6% and 54.7%, respectively. MR and CT sensitivity were 42.6% and 25.0%, while their specificity was 74.1% and 41.3%, respectively. The positive predictive value and negative predictive value of MR and CT were 61.1% and 51.4%, 57.1% and 66.7%, respectively. c2-test showed that MR diagnosis result was consistent with histopathological result (p < 0.05). The coincidence rate of MR and CT evaluation on 5-year disease-free survival and overall survival were 56.7% and 43.8%, respectively. CONCLUSIONS: MR showed a better effect on prognosis than CT and could be treated as the first choice to predict LNR and prognosis. MR demonstrated a good correlation with pathological results and could be used to predict LNR and prognosis.

Memory-built-in quantum cloning in a hybrid solid-state spin register.

As a way to circumvent the quantum no-cloning theorem, approximate quantum cloning protocols have received wide attention with remarkable applications. Copying of quantum states to memory qubits provides an important strategy for eavesdropping in quantum cryptography. We report an experiment that realizes cloning of quantum states from an electron spin to a nuclear spin in a hybrid solid-state spin register with near-optimal fidelity. The nuclear spin provides an ideal memory qubit at room temperature, which stores the cloned quantum states for a millisecond under ambient conditions, exceeding the lifetime of the original quantum state carried by the electron spin by orders of magnitude. The realization of a cloning machine with built-in quantum memory provides a key step for application of quantum cloning in quantum information science.

Experimental realization of universal geometric quantum gates with solid-state spins.

Experimental realization of a universal set of quantum logic gates is the central requirement for the implementation of a quantum computer. In an 'all-geometric' approach to quantum computation, the quantum gates are implemented using Berry phases and their non-Abelian extensions, holonomies, from geometric transformation of quantum states in the Hilbert space. Apart from its fundamental interest and rich mathematical structure, the geometric approach has some built-in noise-resilience features. On the experimental side, geometric phases and holonomies have been observed in thermal ensembles of liquid molecules using nuclear magnetic resonance; however, such systems are known to be non-scalable for the purposes of quantum computing. There are proposals to implement geometric quantum computation in scalable experimental platforms such as trapped ions, superconducting quantum bits and quantum dots, and a recent experiment has realized geometric single-bit gates in a superconducting system. Here we report the experimental realization of a universal set of geometric quantum gates using the solid-state spins of diamond nitrogen-vacancy centres. These diamond defects provide a scalable experimental platform with the potential for room-temperature quantum computing, which has attracted strong interest in recent years. Our experiment shows that all-geometric and potentially robust quantum computation can be realized with solid-state spin quantum bits, making use of recent advances in the coherent control of this system.

Cost-effectiveness of the Health X Project for tuberculosis control in China.

BACKGROUND: Between 2002 and 2008, China's National Tuberculosis Control Programme created the Health X Project, financed in part by a World Bank loan, with additional funding from the UK Department for International Development. OBJECTIVES: To assess the cost-effectiveness of the Project and its impact from a financial point of view on tuberculosis (TB) control in China. METHODS: A decision-analytic model was used to evaluate the cost-effectiveness of the Project. Sensitivity analysis was used to assess the impact of different scenarios and assumptions on results. The primary outcome of the study was cost per disability-adjusted life-year (DALY) saved and incremental DALYs saved. RESULTS: In comparison with alternative scenario 1, the Project detected 1.6 million additional cases, 44 000 deaths were prevented and a total of 18.4 million DALYs saved. The Project strategies cost approximately Chinese yuan (CNY) 953 per DALY saved (vs. CNY1140 in the control areas), and saved an estimated CNY17.5 billion in comparison with the unchanged alternative scenario (scenario 1) or CNY10.8 billion with the control scenario (scenario 2). CONCLUSION: The Project strategies were affordable and of comparable cost-effectiveness to those of other developing countries. The results also provide strong support for the existing policy of scaling up DOTS in China.

SV40 T/t-common polypeptide inhibits angiogenesis and growth of HER2-overexpressing human ovarian cancer.

Human epidermal growth factor receptor 2 (HER2) is frequently overexpressed in human ovarian cancers and its overexpression is associated with increased angiogenesis, increased metastasis and reduced survival. Inhibition of HER2 in HER2-overexpressing cancers can lead to reduced angiogenesis and improved survival. Previously, we reported that SV40 T/t-common polypeptide has transcriptional repression activity and can inhibit HER2 expression. In this study, we investigated the effect of T/t-common on the angiogenesis-inducing activity of HER2-overexpressing human SK-OV-3 ovarian cancer cells. We found that compared to conditioned medium from control SK-OV-3 cancer cells, conditioned medium from T/t-common-expressing SK-OV-3 cells had a reduced ability to induce endothelial cell migration and tube formation in vitro and microvessel formation in vivo. These data indicate that T/t-common can inhibit the ability of SK-OV-3 cancer cells to induce angiogenesis. T/t-common was found to be able to downregulate the expression of several proangiogenic factors, including vascular endothelial growth factor-A, interleukin-8, basic fibroblast growth factor, matrix metalloproteinase-2 and urokinase-type plasminogen activator, and upregulate antiangiogenic factors, including thrombospondin-1 and tissue inhibitor of metalloproteinases-1 in SK-OV-3 cancer cells. Finally, we demonstrated that T/t-common could inhibit the angiogenesis and growth of HER2-overexpressing human ovarian tumor in NOD/SCID mice. Taken together, the data suggest that T/t-common had the potential to be developed as a new antiangiogenic agent specific for treating HER2-overexpressing ovarian cancers.

Molecular characterization of two novel mutations causing factor X deficiency in a Chinese pedigree.

Factor X (FX) deficiency is a rare bleeding disorder inherited as an autosomal recessive trait. In this study, we investigated the molecular basis of FX deficiency in a Chinese pedigree. The proposita showed a markedly prolonged activated partial thromboplastin time and a mild prolongation of prothrombin time. The levels of FX antigen and FX activity were 58.6% and 2.5%, respectively. Molecular analysis revealed that the proposita was compound heterozygous for two novel mutations: IVS1 + 1G > A and G1185A (Arg347His). The aberrant transcripts from the IVS1 + 1G > A mutant allele were not detected by analyzing the splicing pattern of ectopic transcripts in leukocytes of the patient with nested polymerase chain reaction after reverse transcription. We thus hypothesize that the mRNA molecules originating from the IVS1 + 1G > A mutation were rapidly destroyed in vivo. Site-directed mutagenesis of FX cDNA was used to introduce FXG1185A mutation, and wild-type as well as mutant FX proteins were expressed by transient transfection in HEK 293 cells. Normal FX antigen levels both in the conditioned media of cells expressing the mutant and in cell lysates were detected by an enzyme-linked immunoadsorbent assay. Evaluation of wild-type and mutant coagulant activity demonstrated that the FX molecules carrying the Arg347His mutation have dramatically decreased activity.

Identification of three F5 gene mutations associated with inherited coagulation factor V deficiency in two Chinese pedigrees.

To investigate the molecular defects in two Chinese pedigrees with inherited factor V (FV) deficiency. A 37-year-old male (proband 1) and an 18-month-old boy (proband 2) were diagnosed as inherited coagulation FV deficiency by severely reduced plasma levels of FV activity and antigen. All 25 exons and their flanking sequence of F5 gene were amplified by polymerase chain reaction (PCR) for both probands and the PCR products were directly sequenced. Total RNA was extracted from the peripheral lymphocytes of proband 1 for detecting the changes at mRNA level. The homozygous deletion IVS8 -2A>G was identified in the F5 gene of proband 1 and complementary DNA (cDNA) analysis revealed the abolishment of the canonical splicing site by the mutation and the activation of the cryptic acceptor site 24 bp upstream instead. The insertion introduced eight additional amino acids (AA) into the FV protein. Two heterozygous mutations of F5 gene were discovered in proband 2. The 2238-9del AG in exon 13 introduced a premature termination code at 689 AA and the substitution of G6410 by T in exon 23 lead to the missense mutation Gly2079Val. Three F5 gene mutations, IVS8 -2A>G, 2238-9del AG and G6410T, have been identified in two Chinese pedigree with congenital FV deficiency, respectively.

Characterisation of p-nitrophenylglycerol-resistant Proteus mirabilis super-swarming mutants.

p-Nitrophenylglycerol (PNPG) inhibits the co-ordinately regulated activities of swarming behaviour and virulence factor expression in Proteus mirabilis. The inhibitory action of PNPG was investigated by the isolation of Tn5 insertion mutants that could swarm, albeit with much reduced ability, in the presence of PNPG. The mutants exhibited a super-swarming phenotype in the absence of PNPG; i.e., they migrated further in a given time than did the wild-type cells. Cloning and sequence analysis of the mutants indicated that Tn5 was inserted into the rsbA gene, which may encode a membrane sensor histidine kinase of the bacterial two-component signalling system. In the absence of PNPG, the mutants exhibited several swarming-related phenotypes that were different from those of the wild type; they initiated swarming earlier and had a less conspicuous consolidation phase, they differentiated earlier and maintained a differentiated state for longer, they started to express virulence factors earlier and maintained high expression levels of these factors for longer, and they had higher cell invasion ability than the wild type. These mutant phenotypes could be complemented by a plasmid-borne copy of rsbA. Together, these data suggest that RsbA may act as a repressor of swarming and virulence factor expression. In the presence of PNPG, these rsbA-mutated mutants could still swarm, differentiate and express virulence factors, whereas the wild type could not, suggesting that PNPG may target RsbA or RsbA-regulated pathways to exert its inhibitory effect. Together, these data reveal a novel mechanism through which bacteria may negatively regulate swarming differentiation and virulence factor expression and identify a potential target of PNPG action.

Inhibition of virulence factor expression and swarming differentiation in Proteus mirabilis by p-nitrophenylglycerol.

Proteus mirabilis is a common cause of upper urinary tract infections that can involve invasion of host urothelial cells. The ability to invade urothelial cells is coupled closely to swarming, a form of multicellular behaviour in which vegetative bacteria differentiate into hyperflagellate, filamentous swarming cells capable of co-ordinated and rapid population migration. Co-ordinate expression of virulence factors including urease, protease, haemolysin and flagellin during swarm-cell differentiation in P. mirabilis has been reported. To investigate the effects of p-nitrophenylglycerol (PNPG), a potent anti-swarming agent, on the various swarming-associated traits of P. mirabilis and to elucidate the relationships among them, P. mirabilis growth rate, swarming/swimming activity, cell invasion ability and the ability to express various virulence factors were monitored in the presence or absence of PNPG. It was found that PNPG could inhibit the growth rate, swarming differentiation and swarming/swimming activities of P. mirabilis. The expression of virulence factors such as protease, urease, haemolysin and flagellin in P. mirabilis was also inhibited by PNPG. The ability of P. mirabilis to invade human urothelial cells was reduced dramatically in the presence of PNPG. These results suggest that PNPG has the potential to be developed as an agent active against the effects of P. mirabilis infection.