Trade, foreign direct investment and economic growth in Asian economies

Despite the increasing role of foreign direct investment (FDI) in economic development, very limited research has been carried out on the causal links between trade, FDI and economic growth in Asian economies. This study examines empirically the interplay between exports, imports, FDI and economic growth for nine Asian economies by conducting multivariate causality tests in the VECM framework. The results reveal two-way causal connections between trade, inward FDI, inward merger and acquisitions (M&As), and growth for most of the sample economies. There is a unidirectional causal link running from outward M&As to growth and trade. These findings suggest that export expansion, import liberalisation, FDI inflows and inward M&As are integral elements of the growth process in Asian economies

Central limit theorems for high dimensional dependent data

Motivated by statistical inference problems in high-dimensional time series data analysis, we first derive non-asymptotic error bounds for Gaussian approximations of sums of high-dimensional dependent random vectors on hyper-rectangles, simple convex sets and sparsely convex sets. We investigate the quantitative effect of temporal dependence on the rates of convergence to a Gaussian random vector over three different dependency frameworks ($\alpha$-mixing, $m$-dependent, and physical dependence measure). In particular, we establish new error bounds under the $\alpha$-mixing framework and derive faster rate over existing results under the physical dependence measure. To implement the proposed results in practical statistical inference problems, we also derive a data-driven parametric bootstrap procedure based on a kernel estimator for the long-run covariance matrices. We apply the unified Gaussian and bootstrap approximation results to test mean vectors with combined $\ell^2$ and $\ell^\infty$ type statistics, change point detection, and construction of confidence regions for covariance and precision matrices, all for time series data

CFTR Gating II: Effects of Nucleotide Binding on the Stability of Open States

Previously, we demonstrated that ADP inhibits cystic fibrosis transmembrane conductance regulator (CFTR) opening by competing with ATP for a binding site presumably in the COOH-terminal nucleotide binding domain (NBD2). We also found that the open time of the channel is shortened in the presence of ADP. To further study this effect of ADP on the open state, we have used two CFTR mutants (D1370N and E1371S); both have longer open times because of impaired ATP hydrolysis at NBD2. Single-channel kinetic analysis of ΔR/D1370N-CFTR shows unequivocally that the open time of this mutant channel is decreased by ADP. ΔR/E1371S-CFTR channels can be locked open by millimolar ATP with a time constant of ∼100 s, estimated from current relaxation upon nucleotide removal. ADP induces a shorter locked-open state, suggesting that binding of ADP at a second site decreases the locked-open time. To test the functional consequence of the occupancy of this second nucleotide binding site, we changed the [ATP] and performed similar relaxation analysis for E1371S-CFTR channels. Two locked-open time constants can be discerned and the relative distribution of each component is altered by changing [ATP] so that increasing [ATP] shifts the relative distribution to the longer locked-open state. Single-channel kinetic analysis for ΔR/E1371S-CFTR confirms an [ATP]-dependent shift of the distribution of two locked-open time constants. These results support the idea that occupancy of a second ATP binding site stabilizes the locked-open state. This binding site likely resides in the NH(2)-terminal nucleotide binding domain (NBD1) because introducing the K464A mutation, which decreases ATP binding affinity at NBD1, into E1371S-CFTR shortens the relaxation time constant. These results suggest that the binding energy of nucleotide at NBD1 contributes to the overall energetics of the open channel conformation

Constraints on hard spectator scattering and annihilation corrections in Bu,dB_{u,d} →{\to} PVPV decays within QCD factorization

In this paper, we investigate the contributions of hard spectator scattering and annihilation in $B\to PV$ decays within the QCD factorization framework. With available experimental data on $B\to \pi K^{\ast}$, $\rho K$, $\pi \rho$ and $K\phi$ decays, comprehensive $\chi^2$ analyses of the parameters $X_{A,H}^{i,f}({\rho}_{A,H}^{i,f},{\phi}_{A,H}^{i,f})$ are performed, where $X_A^f$ ($X_A^i$) and $X_H$ are used to parameterize the endpoint divergences of the (non)factorizable annihilation and hard spectator scattering amplitudes, respectively. Based on $\chi^2$ analyses, it is observed that (1) The topology-dependent parameterization scheme is feasible for $B\to PV$ decays; (2) At the current accuracy of experimental measurements and theoretical evaluations, $X_H=X_A^i$ is allowed by $B\to PV$ decays, but $X_{H}\neq X_A^f$ at $68$ C. L.; (3) With the simplification $X_H=X_A^i$, parameters $X_A^f$ and $X_A^i$ should be treated individually. The above-described findings are very similar to those obtained from $B\to PP$ decays. Numerically, for $B\to PV$ decays, we obtain $(\rho_{A,H}^i,\phi_{A,H}^i[^{\circ}]) =(2.87^{+0.66}_{-1.95}, -145^{+14}_{-21})$ and $(\rho_A^f,\phi_A^f[^{\circ}]) = (0.91^{+0.12}_{-0.13}, -37^{+10}_{-9})$ at $68$ C. L.. With the best-fit values, most of the theoretical results are in good agreement with the experimental data within errors. However, significant corrections to the color-suppressed tree amplitude $\alpha_2$ related to a large $\rho_H$ result in the wrong sign for $A^{dir}_{CP}(B^- \to \pi^0 K^{{\ast}-})$ compared with the most recent BABAR data, which presents a new obstacle in solving "$\pi\pi$" and "$\pi K$" puzzles through $\alpha_2$. A crosscheck with measurements at Belle (or Belle II) and LHCb, which offer higher precision, is urgently expected to confirm or refute such possible mismatch.Comment: 17 pages, 4 figures; Accepted for publication in PL

Mutations at the Signature Sequence of CFTR Create a Cd2+-gated Chloride Channel

The canonical sequence LSGGQ, also known as the signature sequence, defines the adenosine triphosphate (ATP)-binding cassette transporter superfamily. Crystallographic studies reveal that the signature sequence, together with the Walker A and Walker B motifs, forms the ATP-binding pocket upon dimerization of the two nucleotide-binding domains (NBDs) in a head-to-tail configuration. The importance of the signature sequence is attested by the fact that a glycine to aspartate mutation (i.e., G551D) in cystic fibrosis transmembrane conductance regulator (CFTR) results in a severe phenotype of cystic fibrosis. We previously showed that the G551D mutation completely eliminates ATP-dependent gating of the CFTR chloride channel. Here, we report that micromolar [Cd2+] can dramatically increase the activity of G551D-CFTR in the absence of ATP. This effect of Cd2+ is not seen in wild-type channels or in G551A. Pretreatment of G551D-CFTR with the cysteine modification reagent 2-aminoethyl methane thiosulfonate hydrobromide protects the channel from Cd2+ activation, suggesting an involvement of endogenous cysteine residue(s) in mediating this effect of Cd2+. The mutants G551C, L548C, and S549C, all in the signature sequence of CFTR's NBD1, show robust response to Cd2+. On the other hand, negligible effects of Cd2+ were seen with T547C, Q552C, and R553C, indicating that a specific region of the signature sequence is involved in transmitting the signal of Cd2+ binding to the gate. Collectively, these results suggest that the effect of Cd2+ is mediated by a metal bridge formation between yet to be identified cysteine residue(s) and the engineered aspartate or cysteine in the signature sequence. We propose that the signature sequence serves as a switch that transduces the signal of ligand binding to the channel gate