Learning many-body Hamiltonians with Heisenberg-limited scaling

Learning a many-body Hamiltonian from its dynamics is a fundamental problem in physics. In this work, we propose the first algorithm to achieve the Heisenberg limit for learning an interacting $N$-qubit local Hamiltonian. After a total evolution time of $\mathcal{O}(\epsilon^{-1})$, the proposed algorithm can efficiently estimate any parameter in the $N$-qubit Hamiltonian to $\epsilon$-error with high probability. The proposed algorithm is robust against state preparation and measurement error, does not require eigenstates or thermal states, and only uses $\mathrm{polylog}(\epsilon^{-1})$ experiments. In contrast, the best previous algorithms, such as recent works using gradient-based optimization or polynomial interpolation, require a total evolution time of $\mathcal{O}(\epsilon^{-2})$ and $\mathcal{O}(\epsilon^{-2})$ experiments. Our algorithm uses ideas from quantum simulation to decouple the unknown $N$-qubit Hamiltonian $H$ into noninteracting patches, and learns $H$ using a quantum-enhanced divide-and-conquer approach. We prove a matching lower bound to establish the asymptotic optimality of our algorithm.Comment: 11 pages, 1 figure + 27-page appendi

Local minima in quantum systems

Finding ground states of quantum many-body systems is known to be hard for both classical and quantum computers. As a result, when Nature cools a quantum system in a low-temperature thermal bath, the ground state cannot always be found efficiently. Instead, Nature finds a local minimum of the energy. In this work, we study the problem of finding local minima in quantum systems under thermal perturbations. While local minima are much easier to find than ground states, we show that finding a local minimum is computationally hard for classical computers, even when the task is to output a single-qubit observable at any local minimum. In contrast, we prove that a quantum computer can always find a local minimum efficiently using a thermal gradient descent algorithm that mimics the cooling process in Nature. To establish the classical hardness of finding local minima, we consider a family of two-dimensional Hamiltonians such that any problem solvable by polynomial-time quantum algorithms can be reduced to finding ground states of these Hamiltonians. We prove that for such Hamiltonians, all local minima are global minima. Therefore, assuming quantum computation is more powerful than classical computation, finding local minima is classically hard and quantumly easy.Comment: 9+80 pages, 4 figure

Mutations in the PKM2 exon-10 region are associated with reduced allostery and increased nuclear translocation.

PKM2 is a key metabolic enzyme central to glucose metabolism and energy expenditure. Multiple stimuli regulate PKM2's activity through allosteric modulation and post-translational modifications. Furthermore, PKM2 can partner with KDM8, an oncogenic demethylase and enter the nucleus to serve as a HIF1α co-activator. Yet, the mechanistic basis of the exon-10 region in allosteric regulation and nuclear translocation remains unclear. Here, we determined the crystal structures and kinetic coupling constants of exon-10 tumor-related mutants (H391Y and R399E), showing altered structural plasticity and reduced allostery. Immunoprecipitation analysis revealed increased interaction with KDM8 for H391Y, R399E, and G415R. We also found a higher degree of HIF1α-mediated transactivation activity, particularly in the presence of KDM8. Furthermore, overexpression of PKM2 mutants significantly elevated cell growth and migration. Together, PKM2 exon-10 mutations lead to structure-allostery alterations and increased nuclear functions mediated by KDM8 in breast cancer cells. Targeting the PKM2-KDM8 complex may provide a potential therapeutic intervention

All-trans retinoic acid ameliorates glycemic control in diabetic mice via modulating pancreatic islet production of vascular endothelial growth factor-A.

Patients with type 1 diabetes mellitus are associated with impairment in vitamin A metabolism. This study evaluated whether treatment with retinoic acid, the biologically active metabolite of vitamin A, can ameliorate diabetes. All-trans retinoic acid (atRA) was used to treat streptozotocin (STZ)-induced diabetic mice which revealed atRA administration ameliorated blood glucose levels of diabetic mice. This hyperglycemic amelioration was accompanied by an increase in the amount of β cells co-expressed Pdx1 and insulin and by restoration of the vascular laminin expression. The atRA-induced production of vascular endothelial growth factor-A from the pancreatic islets was possibly the key factor that mediated the restoration of islet vascularity and recovery of β-cell mass. Furthermore, the combination of islet transplantation and atRA administration significantly rescued hyperglycemia in diabetic mice. These findings suggest that vitamin A derivatives can potentially be used as a supplementary treatment to improve diabetes management and glycemic control

Taiwanese Dermatological Association consensus for the management of atopic dermatitis

AbstractBackground/ObjectiveThis report describes the 2014 consensus of the Taiwanese Dermatological Association (TDA) regarding the treatment of atopic dermatitis (AD). The TDA consensus is distributed to practices throughout Taiwan to provide recommendations for therapeutic approaches for AD patients to improve their quality of life.MethodsThe information in the consensus was agreed upon by a panel of national experts at TDA AD consensus meetings held on March 16, May 4, and June 29, 2014. The consensus was in part based on the 2013 Asia–Pacific AD guidelines and the guidelines of the American Academy of Dermatology, with modification to reflect the clinical practice in Taiwan.ResultsThe amendments were drafted after scientific discussions focused on the quality of evidence, risk, and benefits; all the consensus contents were voted on by the participating dermatologists, with approval by at least 75% for inclusion.ConclusionThe consensus provides a comprehensive overview of treatment for AD, with some local and cultural considerations for practitioners in Taiwan, especially the use of wet dressings/wraps, systemic immunomodulatory agents, and complementary therapies

Gfi-1 is the transcriptional repressor of SOCS1 in acute myeloid leukemia cells

ABSTRACT Silencing of SOCS1, a TSG, has been detected in various malignancies, including AML. However, the underlying mechanism of SOCS1 inactivation remains elusive. In this study, we explored the role of histone methylation in SOCS1 expression in AML cells. By ChIP assay, we demonstrated that G9a and SUV39H1, two enzymes catalyzing H3K9 methylation, were physically associated with the SOCS1 promoter, and treatment with chaetocin, a histone methyltransferase inhibitor, suppressed H3K9 methylation on the SOCS1 promoter and enhanced SOCS1 expression. Furthermore, knockdown of G9a and SUV39H1 by siRNA could also induce SOCS1 expression. On the other hand, SOCS1 knockdown by shRNA eliminated chaetocin-induced cell apoptosis. To investigate further whether any transcription factor was involved in H3K9 methylation-related SOCS1 repression, we scanned the sequences of the SOCS1 gene promoter and found two binding sites for Gfi-1, a transcription repressor. By DNA pull-down and ChIP assays, we showed that Gfi-1 directly bound the SOCS1 promoter, and ectopic Gfi-1 expression suppressed STAT5-induced SOCS1 promoter activation. In contrast, Gfi-1 knockdown by shRNA enhanced SOCS1 expression and inhibited STAT5 expression. Moreover, the knockdown of G9a completely rescued the repressive effect of Gfi-1 on STAT5A-induced SOCS1 promoter activation. Collectively, our study indicates that the expression of Gfi-1 contributes to SOCS1 silencing in AML cells through epigenetic modification, and suppression of histone methyltransferase can provide new insight in AML therapy. J. Leukoc. Biol. 95: 000 -000; 2014

Seismic Stratigraphic Features of the Late Miocene-Present Unconformities and Related Seismic Units, Northern Offshore Taiwan

We investigate the seismic stratigraphic features offshore northern Taiwan by using newly collected multichannel seismic data. Two significant regional unconformities U1 and U2 have been identified, which further subdivide the sedimentary sequence into three seismic units as SU I, SU II, and SU III. The lowermost seismic unit SU I is a pre-late Miocene sequence, while the middle and upper seismic unit SU II and SU III result from the interactions between the rapid fault-controlled subsidence and the stable thermal-controlled subsidence. We consider that the present-day offshore northern Taiwan is under a post-collisional state and the unconformities U1 and U2 represent a response to the mountain collapse and to the cessation of the regional volcano-tectonic activities. It is not until 1.5 Ma that northern offshore Taiwan became a post-collisional basin and started to receive sediments, with a rapid fault-controlled subsidence. Afterward, the basin became dominated by a stable thermal-controlled subsidence at 0.2 Ma. Although the main volcano-tectonic activities in the northern offshore Taiwan are ceased, modern geophysical and geochemical investigations have suggested that the tectonism and the volcanism are still active and represent potential threatening geohazard