Reconciliation for Satellite-Based Quantum Key Distribution

This thesis reports on reconciliation schemes based on Low-Density Parity-Check (LDPC) codes in Quantum Key Distribution (QKD) protocols. It particularly focuses on a trade-off between the complexity of such reconciliation schemes and the QKD key growth, a trade-off that is critical to QKD system deployments. A key outcome of the thesis is a design of optimised schemes that maximise the QKD key growth based on finite-size keys for a range of QKD protocols. Beyond this design, the other four main contributions of the thesis are summarised as follows. First, I show that standardised short-length LDPC codes can be used for a special Discrete Variable QKD (DV-QKD) protocol and highlight the trade-off between the secret key throughput and the communication latency in space-based implementations. Second, I compare the decoding time and secret key rate performances between typical LDPC-based rate-adaptive and non-adaptive schemes for different channel conditions and show that the design of Mother codes for the rate-adaptive schemes is critical but remains an open question. Third, I demonstrate a novel design strategy that minimises the probability of the reconciliation process being the bottleneck of the overall DV-QKD system whilst achieving a target QKD rate (in bits per second) with a target ceiling on the failure probability with customised LDPC codes. Fourth, in the context of Continuous Variable QKD (CV-QKD), I construct an in-depth optimisation analysis taking both the security and the reconciliation complexity into account. The outcome of the last contribution leads to a reconciliation scheme delivering the highest secret key rate for a given processor speed which allows for the optimal solution to CV-QKD reconciliation

Prediction of tissue-specific cis-regulatory modules using Bayesian networks and regression trees

<p>Abstract</p> <p>Background</p> <p>In vertebrates, a large part of gene transcriptional regulation is operated by cis-regulatory modules. These modules are believed to be regulating much of the tissue-specificity of gene expression.</p> <p>Results</p> <p>We develop a Bayesian network approach for identifying cis-regulatory modules likely to regulate tissue-specific expression. The network integrates predicted transcription factor binding site information, transcription factor expression data, and target gene expression data. At its core is a regression tree modeling the effect of combinations of transcription factors bound to a module. A new unsupervised EM-like algorithm is developed to learn the parameters of the network, including the regression tree structure.</p> <p>Conclusion</p> <p>Our approach is shown to accurately identify known human liver and erythroid-specific modules. When applied to the prediction of tissue-specific modules in 10 different tissues, the network predicts a number of important transcription factor combinations whose concerted binding is associated to specific expression.</p

NOA1 Functions in a Temperature-Dependent Manner to Regulate Chlorophyll Biosynthesis and Rubisco Formation in Rice

NITRIC OXIDE-ASSOCIATED1 (NOA1) encodes a circularly permuted GTPase (cGTPase) known to be essential for ribosome assembly in plants. While the reduced chlorophyll and Rubisco phenotypes were formerly noticed in both NOA1-supressed rice and Arabidopsis, a detailed insight is still necessary. In this study, by using RNAi transgenic rice, we further demonstrate that NOA1 functions in a temperature-dependent manner to regulate chlorophyll and Rubisco levels. When plants were grown at 30°C, the chlorophyll and Rubisco levels in OsNOA1-silenced plants were only slightly lower than those in WT. However, at 22°C, the silenced plants accumulated far less chlorophyll and Rubisco than WT. It was further revealed that the regulation of chlorophyll and Rubisco occurs at the anabolic level. Etiolated WT seedlings restored chlorophyll and Rubisco accumulations readily once returned to light, at either 30°C or 15°C. Etiolated OsNOA1-silenced plants accumulated chlorophyll and Rubisco to normal levels only at 30°C, and lost this ability at low temperature. On the other hand, de-etiolated OsNOA1-silenced seedlings maintained similar levels of chlorophyll and Rubisco as WT, even after being shifted to 15°C for various times. Further expression analyses identified several candidate genes, including OsPorA (NADPH: protochlorophyllide oxidoreductase A), OsrbcL (Rubisco large subunit), OsRALyase (Ribosomal RNA apurinic site specific lyase) and OsPuf4 (RNA-binding protein of the Puf family), which may be involved in OsNOA1-regulated chlorophyll biosynthesis and Rubisco formation. Overall, our results suggest OsNOA1 functions in a temperature-dependent manner to regulate chlorophyll biosynthesis, Rubisco formation and plastid development in rice

Human Placental-Specific Epipolymorphism and its Association with Adverse Pregnancy Outcomes

Interindividual variation in DNA-methylation level is widespread in the human genome, despite its critical role in regulating gene expression. The nature of this variation, including its tissue-specific nature, and the role it may play in human phenotypic variation and disease is still poorly characterized. The placenta plays a critical role in regulating fetal growth and development in ways that have lifelong effects on health. To identify genes with a high degree of interindividual DNA methylation variation in the human placenta, we surveyed the human genome using the Illumina GoldenGate Methylation Cancer panel targeting 1505 CpG sites of 807 genes. While many sites show a continuous pattern of methylation levels, WNT2, TUSC3 and EPHB4 were identified to have a polymorphic “on-or-off” pattern of DNA methylation variation at their promoter region which was confirmed by pyrosequencing. Methylation of these genes can be found in 7%–25% of over 100 placentas tested. The methylation state at the promoter of these genes is concordant with mRNA allelic expression. In three informative cases TUSC3 was observed to be methylated on the maternal allele, and it is thus possible this represents a polymorphically imprinted gene. Furthermore, TUSC3 promoter methylation showed evidence for association with preeclampsia. A biological significance of these methylation allelic polymorphisms (MAPs) to human placental diversity is further implied by their placental specificity and absence in mouse. An extended study of blood suggests that MAPs may also be found in other tissues, implicating their utility for tissue-specific association with complex disorders. The identification of such “epipolymorphism” in other tissues and their use in association studies, should improve our understanding of interindividual phenotypic variability and complex disease susceptibility

Search for a scalar partner of the X(3872)X(3872) via ψ(3770)\psi(3770) decays into γηη′\gamma\eta\eta' and γπ+π−J/ψ\gamma\pi^{+}\pi^{-}J/\psi

Using a data sample corresponding to an integrated luminosity of 2.93 fb$^{-1}$ collected at a center-of-mass energy of 3.773~GeV with the BESIII detector at the BEPCII collider, we search for a scalar partner of the $X(3872)$, denoted as $X(3700)$, via $\psi(3770)\to \gamma\eta\eta'$ and $\gamma\pi^{+}\pi^{-}J/\psi$ processes. No significant signals are observed and the upper limits of the product branching fractions ${\cal B}(\psi(3770)\to\gamma X(3700))\cdot {\cal B}(X(3700)\to \eta\eta')$ and ${\cal B}(\psi(3770)\to\gamma X(3700))\cdot {\cal B}(X(3700)\to\pi^{+}\pi^{-}J/\psi)$ are determined at the 90\% confidence level, for the narrow $X(3700)$ with a mass ranging from 3710 to 3740 MeV/$c^2$, which are from 0.8 to 1.8 $(\times 10^{-5})$ and 0.9 to 3.4 $(\times 10^{-5})$, respectively

Measurement of branching fractions of Λc+\Lambda_{c}^{+} decays to Σ+K+K−\Sigma^{+} K^{+} K^{-}, Σ+ϕ\Sigma^{+}\phi and Σ+K+π−(π0)\Sigma^{+} K^{+} \pi^{-}(\pi^{0})

Based on 4.5 fb$^{-1}$ data taken at seven center-of-mass energies ranging from 4.600 to 4.699 GeV with the BESIII detector at the BEPCII collider, we measure the branching fractions of $\Lambda_{c}^{+}\rightarrow\Sigma^{+}+hadrons$ relative to $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$. Combining with the world average branching fraction of $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$, their branching fractions are measured to be $(0.377\pm0.042\pm0.018\pm0.021)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} K^{-}$, $(0.200\pm0.023\pm0.010\pm0.011)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} \pi^{-}$, $(0.414\pm0.080\pm0.029\pm0.023)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+}\phi$ and $(0.197\pm0.036\pm0.008\pm0.011)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+}K^{+} K^{-}$(non-$\phi$). In all the above results, the first uncertainties are statistical, the second are systematic and the third are from external input of the branching fraction of $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$. Since no signal for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} \pi^{-}\pi^{0}$ is observed, the upper limit of its branching fraction is determined to be 0.11\% at the 90$\%$ confidence level

Evaluating the Effects of SARS-CoV-2 Spike Mutation D614G on Transmissibility and Pathogenicity.

Global dispersal and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of a selective advantage but may also be due to a random founder effect. We investigate the hypothesis for positive selection of spike D614G in the United Kingdom using more than 25,000 whole genome SARS-CoV-2 sequences. Despite the availability of a large dataset, well represented by both spike 614 variants, not all approaches showed a conclusive signal of positive selection. Population genetic analysis indicates that 614G increases in frequency relative to 614D in a manner consistent with a selective advantage. We do not find any indication that patients infected with the spike 614G variant have higher COVID-19 mortality or clinical severity, but 614G is associated with higher viral load and younger age of patients. Significant differences in growth and size of 614G phylogenetic clusters indicate a need for continued study of this variant

Measurement of the cross section of e+e−→Ξ−Ξˉ+e^+e^-\rightarrow\Xi^{-}\bar\Xi^{+} at center-of-mass energies between 3.510 and 4.843 GeV

Using $e^+e^-$ collision data corresponding to a total integrated luminosity of 12.9 $fb^{-1}$ collected with the BESIII detector at the BEPCII collider, the exclusive Born cross sections and the effective form factors of the reaction $e^+e^-\rightarrow\Xi^{-}\bar\Xi^{+}$ are measured via the single baryon-tag method at 23 center-of-mass energies between 3.510 and 4.843 GeV. Evidence for the decay $\psi(3770)\rightarrow\Xi^{-}\bar\Xi^{+}$ is observed with a significance of 4.5$\sigma$ by analyzing the measured cross sections together with earlier BESIII results. For the other charmonium(-like) states $\psi(4040)$, $\psi(4160)$, $Y(4230)$, $Y(4360)$, $\psi(4415)$, and $Y(4660)$, no significant signal of their decay to $\Xi^-\bar \Xi^+$ is found. For these states, upper limits of the products of the branching fraction and the electronic partial width at the 90% confidence level are provided.Comment: 18 pages, 10 pages, 4 table