In this paper, we propose a quantum algorithm that supports a real-valued higher-order unconstrained binary optimization (HUBO) problem. This algorithm is based on the Grover adaptive search that ...originally supported HUBO with integer coefficients. Next, as an application example, we formulate multiple-input multiple-output maximum likelihood detection as a HUBO problem with real-valued coefficients, where we use the Gray-coded bit-to-symbol mapping specified in the 5G standard. The proposed approach allows us to construct an efficient quantum circuit for the detection problem and to analyze specific numbers of required qubits and quantum gates, whereas other conventional studies have assumed that such a circuit is feasible as a quantum oracle. To further accelerate the quantum algorithm, we also derive a probability distribution of the objective function value and determine a unique threshold to sample better states. Assuming a future fault-tolerant quantum computing, our proposed algorithm has the potential for significantly reducing query complexity in the classical domain and providing a quadratic speedup in the quantum domain.
Maximum-likelihood multiuser detection incurs a large computational complexity, and its low-complexity detection scheme suffers from a performance loss, where this tradeoff is inevitable and inherent ...in a classical computer. In this paper, we use the Grover adaptive search (GAS) to break the tradeoff, which is a quantum exhaustive search algorithm guaranteed to obtain the optimal solution, achieving a quadratic speedup. Specifically, we design two specific parameters of GAS to achieve the optimal performance with a reduced complexity: the initial threshold and the number of Grover rotations. The initial threshold of GAS can be optimized using a solution of semi-definite programming, and it is possible to calculate the distribution of the number of solutions smaller than the initial threshold in advance, which depends on instantaneous channel coefficients. In addition, we analyze the number of quantum gates required for GAS and show that the gate count can be reduced by bypassing the higher-order terms in the objective function, leading to a reduced circuit runtime. Our analysis and simulation results demonstrate that the proposed approach achieves the same performance as the optimal maximum-likelihood detection while reducing the query complexity of GAS, implying that the large constant overhead of quadratic speedup can be further reduced.
In this article, we propose a novel method of formulating an NP-hard wireless channel assignment problem as a higher-order unconstrained binary optimization (HUBO), where the Grover adaptive search ...(GAS) is used to provide a quadratic speedup for solving the problem. The conventional method relies on a one-hot encoding of the channel indices, resulting in a quadratic formulation. By contrast, we conceive ascending and descending binary encodings of the channel indices, construct a specific quantum circuit, and derive the exact numbers of qubits and gates required by GAS. Our analysis clarifies that the proposed HUBO formulation significantly reduces the number of qubits and the query complexity compared with the conventional quadratic formulation. This advantage is achieved at the cost of an increased number of quantum gates, which we demonstrate can be reduced by our proposed descending binary encoding.
In this paper, we propose a novel method of formulating an NP-hard wireless channel assignment problem as a higher-order unconstrained binary optimization (HUBO), where the Grover adaptive search ...(GAS) is used to provide a quadratic speedup for solving the problem. The conventional method relies on a one-hot encoding of the channel indices, resulting in a quadratic formulation. By contrast, we conceive ascending and descending binary encodings of the channel indices, construct a specific quantum circuit, and derive the exact numbers of qubits and gates required by GAS. Our analysis clarifies that the proposed HUBO formulation significantly reduces the number of qubits and the query complexity compared with the conventional quadratic formulation. This advantage is achieved at the cost of an increased number of quantum gates, which we demonstrate can be reduced by our proposed descending binary encoding.
In this paper, we propose a quantum algorithm that supports a real-valued higher-order unconstrained binary optimization (HUBO) problem. This algorithm is based on the Grover adaptive search that ...originally supported HUBO with integer coefficients. Next, as an application example, we formulate multiple-input multiple-output maximum likelihood detection as a HUBO problem with real-valued coefficients, where we use the Gray-coded bit-to-symbol mapping specified in the 5G standard. The proposed approach allows us to construct an efficient quantum circuit for the detection problem and to analyze specific numbers of required qubits and quantum gates, whereas other conventional studies have assumed that such a circuit is feasible as a quantum oracle. To further accelerate the quantum algorithm, we also derive a probability distribution of the objective function value and determine a unique threshold to sample better states. Assuming a future fault-tolerant quantum computing, our proposed algorithm has the potential for significantly reducing query complexity in the classical domain and providing a quadratic speedup in the quantum domain.
In this article, we propose a novel method of formulating an NP-hard wireless channel assignment problem as a higher-order unconstrained binary optimization (HUBO), where the Grover adaptive search ...(GAS) is used to provide a quadratic speedup for solving the problem. The conventional method relies on a one-hot encoding of the channel indices, resulting in a quadratic formulation. By contrast, we conceive ascending and descending binary encodings of the channel indices, construct a specific quantum circuit, and derive the exact numbers of qubits and gates required by GAS. Our analysis clarifies that the proposed HUBO formulation significantly reduces the number of qubits and the query complexity compared with the conventional quadratic formulation. This advantage is achieved at the cost of an increased number of quantum gates, which we demonstrate can be reduced by our proposed descending binary encoding.
It is well known that sensitization against fungi is closely associated with severity of asthma. Dectin-1 (gene symbol Clec7a), a C-type lectin receptor, recognizes the fungal cell wall component ...β-glucan, as well as some component(s) in house dust mite (HDM) extract. However, the roles of Dectin-1 in HDM-induced allergic airway inflammation remain unclear. In this study, we used Dectin-1-deficient (Clec7a
) mice to examine whether Dectin-1 is involved in HDM-induced allergic airway inflammation. We found that HDM-induced eosinophil and neutrophil recruitment into the airways was significantly attenuated in Clec7a
mice compared with that in wild-type mice. In addition, HDM-induced IL-5, IL-13, and IL-17 production from mediastinum lymph node cells was reduced in HDM-sensitized Clec7a
mice. Dectin-1 was expressed on CD11b
dendritic cells (DCs), an essential DC subset for the development of allergic inflammation, but not on CD103
DCs, plasmacytoid DCs, or lung epithelial cells. Transcriptome analysis revealed that the expression of chemokine/chemokine receptors, including CCR7, which is indispensable for DC migration to draining lymph nodes, was decreased in Clec7a
DCs. In accordance with these results, the number of HDM-labeled CD11b
DCs in mediastinum lymph nodes was significantly reduced in Clec7a
mice compared with wild-type mice. Taken together, these results suggest that Dectin-1 expressed on CD11b
DCs senses some molecule(s) in HDM extract and plays a critical role in the induction of HDM-induced allergic airway inflammation by inducing the expression of chemokine/chemokine receptors in DCs.
The fact that sensitization against fungi is closely related to the severity of asthma suggests that immune systems recognizing fungi are involved in the pathogenesis of severe asthma. Recently, ...Dectin-2 (gene symbol, Clec4n), a C-type lectin receptor, has been shown to function as not only a major pattern-recognition receptor for fungi, but also a receptor for some components of house dust mite (HDM) extract, a major allergen for asthma. However, the roles of Dectin-2 in the induction of HDM-induced allergic airway inflammation remain largely unknown. Our objective was to determine the roles of Dectin-2 in HDM-induced allergic airway inflammation. We examined the roles of Dectin-2 in the induction of HDM-induced T helper (Th) 2 and Th17 cell differentiation and subsequent allergic airway inflammation by using Clec4n-deficient (Clec4n(-/-)) mice. We also investigated Dectin-2-expressing cells in the lung and their roles in HDM-induced allergic airway inflammation. Clec4n(-/-) mice showed significantly attenuated HDM-induced allergic airway inflammation and decreased Th2 and Th17 cell differentiation. Dectin-2 mRNA, together with Dectin-3 and Fc receptor-γ mRNAs, was expressed in CD11b(+) dendritic cells (DCs), but not in CD4(+) T cells or epithelial cells in the lung. CD11b(+) DCs isolated from Clec4n(-/-) mice expressed lower amounts of proinflammatory cytokines and costimulatory molecules, which could lead to Th2 and Th17 cell differentiation than those from wild-type mice. HDM-pulsed Clec4n(-/-) DCs were less efficient for the induction of allergic airway inflammation than HDM-pulsed wild-type DCs. In conclusion, Dectin-2 expressed on CD11b(+) DCs promotes HDM-induced Th2 and Th17 cell differentiation and allergic airway inflammation.
The relationship between class switch recombination (CSR) and somatic hypermutation has been unclear. By using human CD27− naive B cells, we investigated the somatic hypermutation and producibility ...of immunoglobulins (Igs) that occur after CSR. Although neither adult CD27− nor cord blood B cells, which showed the unmutated Ig V-region genes, produced IgG, IgM, or IgA in response to conventional stimuli, they produced IgG and IgM but not IgA in the presence of Staphylococcus aureus Cowan strain (SAC) + interleukin-2 (IL-2) + IL-10 + anti-CD40 mAb + CD32 transfectants (CD40/CD32T). The naive B cells also produced IgE when combined with IL-4 + CD40/CD32T. In parallel with IgG production, the expression of mature γ1 and γ 2 transcripts was induced from naive B cells by the stimuli. The CD27 expression on human naive B cells was induced remarkably by CD40 signaling or B-cell receptor engagement, but somatic hypermutation could not be induced. The proliferation and differentiation into plasma cells were induced from naive B cells, whereas most of the plasma cells displayed very low levels of mutations in Ig V-region genes. CD27− naive B cells expressed activation-induced cytidine deaminase messenger RNA by the stimuli later than CD27+memory B cells. Our results demonstrate that CSR, but not noticeable somatic hypermutation, can be induced from CD27− naive B cells upon B-cell receptor engagement and CD40 signaling in cooperation with cytokines, suggesting that CSR and somatic hypermutation processes can occur independently, and the antibodies produced in this in vitro system are low-affinity antibodies.
The molecular basis of common variable immunodeficiency (CVID) is unknown. To assess humoral immunity in CVID, we selected 24 patients with early or late onset of disease. X-linked agammaglobulinemia ...(XLA), X-linked hyper-IgM syndrome (XHIM), and non-XHIM were excluded based on clinical phenotype, assessment of the immune response, presence of Bruton's tyrosine kinase (Btk) in monocytes or platelets, and normal expression of CD40 ligand by activated T cells. The number of circulating B cells was within the normal range or reduced. IgD− CD27+ memory B cells were markedly reduced or absent in all 24 patients and IgD+ CD27+ B cells were diminished in 8 patients. Circulating B cells from all 6 patients examined, including CVID patients with IgD+ CD27+ cells, failed to undergo somatic hypermutation in immunoglobulin-variable (V)-region genes, similar to cord blood B cells. B cells from CVID patients produced IgM and IgG, but not IgA upon the engagement of Ig receptor and CD40 in the presence of IL-2 and IL-10. B cells from all but 5 patients secreted IgE when stimulated by CD40 crosslinking in the presence of IL-4. The observation of defective memory B cells with abnormal cell marker expression and function demonstrates that naive CVID B cells including those expressing IgD+ CD27+, in analogy to cord blood and hyper-IgM syndrome B cells, may be responsible for their failure to differentiate into plasma cells and to produce high-affinity antibodies of different isotypes.
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