10 research outputs found

    Signal representations via SIP p-frames and SIP Bessel multipliers in separable Banach spaces

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    Digital signals are often modeled as functions in Banach spaces, such as the ubiquitous [Formula: see text] spaces. The frame theory in Banach spaces induces flexible representations of signals due to the robustness and redundancy of frames. Nevertheless, the lack of inner product in general Banach spaces limits the direct representations of signals in Banach spaces under a given basis or frame. In this paper, we introduce the concept of semi-inner product (SIP) [Formula: see text]-Bessel multipliers to extend the flexibility of signal representations in separable Banach spaces, where [Formula: see text]. These multipliers are defined as composition of analysis operator of an SIP-I Bessel sequence, a multiplication with a fixed sequence and synthesis operator of an SIP-II Bessel sequence. The basic properties of the SIP [Formula: see text]-Bessel multipliers are investigated. Moreover, as special cases, characterizations of [Formula: see text]-Riesz bases related to signal representations are given, and the multipliers for [Formula: see text]-Riesz bases are discussed. We show that SIP [Formula: see text]-Bessel multipliers for [Formula: see text]-Riesz bases are invertible. Finally, the continuity of SIP [Formula: see text]-Bessel multipliers with respect to their parameters is investigated. The results theoretically show that the SIP [Formula: see text]-Bessel multipliers offer a larger range of freedom than frames on signal representations in Banach spaces. </jats:p

    Identification of soybean mosaic virus resistance alleles in Jindou 1 soybean

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    From Grayscale to Color: Quaternion Linear Regression for Color Face Recognition

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    Decades of Genetic Research on Soybean mosaic virus Resistance in Soybean

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    This review summarizes the history and current state of the known genetic basis for soybean resistance to Soybean mosaic virus (SMV), and examines how the integration of molecular markers has been utilized in breeding for crop improvement. SVM causes yield loss and seed quality reduction in soybean based on the SMV strain and the host genotype. Understanding the molecular underpinnings of SMV–soybean interactions and the genes conferring resistance to SMV has been a focus of intense research interest for decades. Soybean reactions are classified into three main responses: resistant, necrotic, or susceptible. Significant progress has been achieved that has greatly increased the understanding of soybean germplasm diversity, differential reactions to SMV strains, genotype–strain interactions, genes/alleles conferring specific reactions, and interactions among resistance genes and alleles. Many studies that aimed to uncover the physical position of resistance genes have been published in recent decades, collectively proposing different candidate genes. The studies on SMV resistance loci revealed that the resistance genes are mainly distributed on three chromosomes. Resistance has been pyramided in various combinations for durable resistance to SMV strains. The causative genes are still elusive despite early successes in identifying resistance alleles in soybean; however, a gene at the Rsv4 locus has been well validated

    Decades of Genetic Research on Soybean mosaic virus Resistance in Soybean

    No full text
    This review summarizes the history and current state of the known genetic basis for soybean resistance to Soybean mosaic virus (SMV), and examines how the integration of molecular markers has been utilized in breeding for crop improvement. SVM causes yield loss and seed quality reduction in soybean based on the SMV strain and the host genotype. Understanding the molecular underpinnings of SMV–soybean interactions and the genes conferring resistance to SMV has been a focus of intense research interest for decades. Soybean reactions are classified into three main responses: resistant, necrotic, or susceptible. Significant progress has been achieved that has greatly increased the understanding of soybean germplasm diversity, differential reactions to SMV strains, genotype–strain interactions, genes/alleles conferring specific reactions, and interactions among resistance genes and alleles. Many studies that aimed to uncover the physical position of resistance genes have been published in recent decades, collectively proposing different candidate genes. The studies on SMV resistance loci revealed that the resistance genes are mainly distributed on three chromosomes. Resistance has been pyramided in various combinations for durable resistance to SMV strains. The causative genes are still elusive despite early successes in identifying resistance alleles in soybean; however, a gene at the Rsv4 locus has been well validated.</jats:p

    Suppressing neutrophil itaconate production attenuates Mycoplasma pneumoniae pneumonia.

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    Mycoplasma pneumoniae is a common cause of community-acquired pneumonia in which neutrophils play a critical role. Immune-responsive gene 1 (IRG1), responsible for itaconate production, has emerged as an important regulator of inflammation and infection, but its role during M. pneumoniae infection remains unknown. Here, we reveal that itaconate is an endogenous pro-inflammatory metabolite during M. pneumoniae infection. Irg1 knockout (KO) mice had lower levels of bacterial burden, lactate dehydrogenase (LDH), and pro-inflammatory cytokines compared with wild-type (WT) controls after M. pneumoniae infection. Neutrophils were the major cells producing itaconate during M. pneumoniae infection in mice. Neutrophil counts were positively correlated with itaconate concentrations in bronchoalveolar lavage fluid (BALF) of patients with severe M. pneumoniae pneumonia. Adoptive transfer of Irg1 KO neutrophils, or administration of β-glucan (an inhibitor of Irg1 expression), significantly attenuated M. pneumoniae pneumonia in mice. Mechanistically, itaconate impaired neutrophil bacterial killing and suppressed neutrophil apoptosis via inhibiting mitochondrial ROS. Moreover, M. pneumoniae induced Irg1 expression by activating NF-κB and STAT1 pathways involving TLR2. Our data thus identify Irg1/itaconate pathway as a potential therapeutic target for the treatment of M. pneumoniae pneumonia
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