Ab initio Quantum Simulation of Strongly Correlated Materials with Quantum Embedding

Quantum computing has shown great potential in various quantum chemical applications such as drug discovery, material design, and catalyst optimization. Although significant progress has been made in quantum simulation of simple molecules, ab initio simulation of solid-state materials on quantum computers is still in its early stage, mostly owing to the fact that the system size quickly becomes prohibitively large when approaching the thermodynamic limit. In this work, we introduce an orbital-based multi-fragment approach on top of the periodic density matrix embedding theory, resulting in a significantly smaller problem size for the current near-term quantum computer. We demonstrate the accuracy and efficiency of our method compared with the conventional methodologies and experiments on solid-state systems with complex electronic structures. These include spin polarized states of a hydrogen chain (1D-H), the equation of states of a boron nitride layer (h-BN) as well as the magnetic ordering in nickel oxide (NiO), a prototypical strongly correlated solid. Our results suggest that quantum embedding combined with a chemically intuitive fragmentation can greatly advance quantum simulation of realistic materials, thereby paving the way for solving important yet classically hard industrial problems on near-term quantum devices.Comment: 14 pages, 5 figures, and 3 table

Antiviral treatment alters the frequency of activating and inhibitory receptor-expressing natural killer cells in chronic Hepatitis B virus infected patients

Natural killer (NK) cells play a critical role in innate antiviral immunity, but little is known about the impact of antiviral therapy on the frequency of NK cell subsets. To this aim, we performed this longitudinal study to examine the dynamic changes of the frequency of different subsets of NK cells in CHB patients after initiation of tenofovir or adefovir therapy. We found that NK cell numbers and subset distribution differ between CHB patients and normal subjects; furthermore, the association was found between ALT level and CD158b+ NK cell in HBV patients. In tenofovir group, the frequency of NK cells increased during the treatment accompanied by downregulated expression of NKG2A and KIR2DL3. In adefovir group, NK cell numbers did not differ during the treatment, but also accompanied by downregulated expression of NKG2A and KIR2DL3. Our results demonstrate that treatment with tenofovir leads to viral load reduction, and correlated with NK cell frequencies in peripheral blood of chronic hepatitis B virus infection. In addition, treatments with both tenofovir and adefovir in chronic HBV infected patients induce a decrease of the frequency of inhibitory receptor+ NK cells, which may account for the partial restoration of the function of NK cells in peripheral blood following treatment

(E)-Methyl N′-(2-furylmethyl­ene)­hydrazinecarboxyl­ate

The title compound, C7H8N2O3, crystallizes with two independent but essentially identical mol­ecules in the asymmetric unit. Each mol­ecule adopts a trans configuration with respect to the C=N bond. The hydrazinecarboxyl­ate group is twisted from the furan ring by 7.78 (13)° in one mol­ecule and by 7.01 (17)° in the other. In the crystal structure, mol­ecules are linked into chains running along [010] by bifurcated N—H⋯(N,O) and N—H⋯O hydrogen bonds. In addition, weak C—H⋯O inter­actions and an O⋯C short contact [2.896 (3) Å] are observed

Biofilm formation and antibiotic sensitivity in Elizabethkingia anophelis

Elizabethkingia anophelis has recently gained global attention and is emerging as a cause of life-threatening nosocomial infections. The present study aimed to investigate the association between antimicrobial resistance and the ability to form biofilm among E. anophelis isolated from hospitalized patients in China. Over 10 years, a total of 197 non-duplicate E. anophelis strains were collected. Antibiotic susceptibility was determined by the standard agar dilution method as a reference assay according to the Clinical and Laboratory Standards Institute. The biofilm formation ability was assessed using a culture microtiter plate method, which was determined using a crystal violet assay. Culture plate results were cross-checked by scanning electron microscopy imaging analysis. Among the 197 isolates, all were multidrug-resistant, and 20 were extensively drug-resistant. Clinical E. anophelis showed high resistance to current antibiotics, and 99% of the isolates were resistant to at least seven antibiotics. The resistance rate for aztreonam, ceftazidime, imipenem, meropenem, trimethoprim-sulfamethoxazole, cefepime, and tetracycline was high as 100%, 99%, 99%, 99%, 99%, 95%, and 90%, respectively. However, the isolates exhibited the highest susceptibility to minocycline (100%), doxycycline (96%), and rifampin (94%). The biofilm formation results revealed that all strains could form biofilm. Among them, the proportions of strong, medium, and weak biofilm-forming strains were 41%, 42%, and 17%, respectively. Furthermore, the strains forming strong or moderate biofilm presented a statistically significant higher resistance than the weak formers (p < 0.05), especially for piperacillin, piperacillin-tazobactam, cefepime, amikacin, and ciprofloxacin. Although E. anophelis was notoriously resistant to large antibiotics, minocycline, doxycycline, and rifampin showed potent activity against this pathogen. The data in the present report revealed a positive association between biofilm formation and antibiotic resistance, which will provide a foundation for improved therapeutic strategies against E. anophelis infections in the future

Timing Is Critical for an Effective Anti-Metastatic Immunotherapy: The Decisive Role of IFNγ/STAT1-Mediated Activation of Autophagy

BACKGROUND: Immunotherapy is often recommended as an adjuvant treatment to reduce the chance of cancer recurrence or metastasis. Interestingly, timing is very important for a successful immunotherapy against metastasis, although the precise mechanism is still unknown. METHODS AND FINDINGS: Using a mouse model of melanoma metastasis induced by intravenous injection of B16-F10 cells, we investigated the mechanism responsible for the diverse efficacy of the prophylactic or therapeutic TLR4 and TLR9 agonist complex against metastasis. We found that the activation of TLR4 and TLR9 prevented, but did not reverse, metastasis because the potency of this combination was neither sufficient to overcome the tumor cell-educated immune tolerance nor to induce efficacious autophagy in tumor cells. The prophylactic application of the complex promoted antimetastatic immunity, leading to the autophagy-associated death of melanoma cells via IFNγ/STAT1 activation and attenuated tumor metastasis. IFNγ neutralization reversed the prophylactic benefit induced by the complex by suppressing STAT1 activation and attenuating autophagy in mice. However, the therapeutic application of the complex did not suppress metastasis because the complex could not reverse tumor cell-induced STAT3 activation and neither activate IFNγ/STAT1 signaling and autophagy. Suppressing STAT3 activation with the JAK/STAT antagonist AG490 restored the antimetastatic effect of the TLR4/9 agonist complex. Activation of autophagy after tumor inoculation by using rapamycin, with or without the TLR4/9 agonist complex, could suppress metastasis. CONCLUSION AND SIGNIFICANCE: Our studies suggest that activation of IFNγ/STAT1 signaling and induction of autophagy are critical for an efficacious anti-metastatic immunotherapy and that autophagy activators may overcome the timing barrier for immunotherapy against metastasis

(E)-Methyl N′-(3,4-dimethoxy­benzyl­idene)hydrazinecarboxyl­ate

The title compound, C11H14N2O4, crystallizes with two independent but essentially identical mol­ecules in the asymmetric unit. Each mol­ecule adopts a trans configuration with respect to the C=N bond. Mol­ecules are linked into a one-dimensional network by inter- and intra­molecular N—H⋯O and C—H⋯O hydrogen bonds

(E)-Ethyl N′-(3,4-dimethoxy­benzyl­idene)hydrazinecarboxyl­ate monohydrate

In the title compound, C12H16N2O4·H2O, the mol­ecular skeleton of the hydrazinecarboxyl­ate is nearly planar [within 0.053 (3) Å]. In the crystal, chains propagating along the c axis arise, composed of alternating hydrazinecarboxyl­ate mol­ecules and crystalline water, which inter­act via N—H⋯O and O—H⋯O hydrogen bonds