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We connected the two ends of a finite spin-1/2 antiferromagnetic Ising chain with a magnetic impurity at one end to form a closed ring, and studied its magnetic susceptibility exactly by using the transfer matrix method. We calculated the magnetic susceptibility in the whole temperature range and gave the phase diagram at ground state of the system about the anisotropy of the impurity and strength of the connection exchange interaction for spin-1 and -3/2 impurities. We also gave the ground state entropy of the system and derived the asymptotic expression of the magnetic susceptibility multiplied by temperature at the zero-temperature limit and the high-temperature limit. It was found that a degenerate phase may exist in some parameter region at zero temperature for the odd spin number system, and the ground state entropy is ln(2) in the nondegenerate phase and is dependent on the spin number in the degenerate phase. The magnetic susceptibility of the system at low temperature exhibits ferromagnetic behavior, and the Curie constant is related to the spin configuration at ground state. When the ground state is nondegenerate, the Curie constant is equal to the square of the net spin, regardless of the parity of the number of the spin. When the spin number is odd and the ground state is degenerate, the Curie constant may be related to the total spin number. At the high-temperature limit, the magnetic susceptibility multiplied by temperature is related to the spin quantum number of the impurity and the spin number in the ring. Key words: transfer matrix method, magnetic susceptibility, magnetic impurity, Ising ring, Curie's law. Nous connectons les deux bouts d'une chaine d'Ising finie de spin 1/2 antiferromagnetique avec une impurete magnetique a un bout, dans le but d'etudier de facon exacte la susceptibilite magnetique en utilisant la methode de la matrice de transfert. Nous calculons la susceptibilite magnetique dans le domaine complet de temperature. Nous presentons aussi le diagramme de phase dans le fondamental du systeme touchant l'anisotropie de l'impurete et la force de l'interaction d'echange, pour les impuretes de spin 1 et 3/2. Nous donnons aussi l'entropie du fondamental du systeme et derivons l'expression asymptotique de la susceptibilite magnetique multipliee par la temperature a la limite de temperature zero et a la limite de haute temperature. Nous trouvons qu'une phase degeneree peut exister dans certaine region parametrique a temperature zero pour un nombre impair de spins du systeme oU l'entropie du fondamental du systeme est ln(2) dans la phase non degeneree, alors qu'elle est dependante du nombre de spin dans la phase degeneree. La susceptibilite magnetique du systeme a basse temperature a un comportement ferromagnetique et la constante de Curie est reliee a la configuration de spin dans l'etat fondamental. Quand le fondamental est non degenere, la constante de Curie est egale au carre du spin net, sans regard au caractere pair/impair du nombre de spins dans l'anneau. Lorsque le nombre de spins est impair et que le fondamental est degenere, la constante de Curie peut etre reliee au nombre total de spins. Dans la limite de haute temperature, la susceptibilite magnetique multipliee par la temperature est reliee au nombre quantique de spin de l'impurete et au nombre de spins dans l'anneau. [Traduit par la Redaction] Mots-cles : methode de la matrice de transfert, susceptibilite magnetique, impurete magnetique, anneau d'Ising, loi de Curie., 1. Introduction In condensed matter physics, the variants of low-dimensional quantum antiferromagnetic system have received much attention due to their low dimensionality and a novel phenomenon arising from the quantum [...]

As a pillar industry with high energy consumption and low efficiency, the building industry of China has produced consistently high carbon emission levels in recent years. The important goals in the coordinated development of this industry include the large-scale development of green buildings, the use of energy technologies to reduce carbon emissions, and an effective reduction of carbon intensity. Prefabricated buildings have become popular in this industry due to their low energy consumption, emission, and pollution and environment-friendly nature. This paper examines those factors that influence the carbon emissions from the construction of prefabricated buildings across three phases, namely, production in plants, logistics transportation, and assembly construction, builds an evaluation index system for studying the carbon emissions in the materialization phase of prefabricated buildings, and employs the hierarchical fuzzy comprehensive evaluation method to construct an evaluation model. Results show that the overall energy consumption of prefabricated buildings is lower than that of traditional concrete pouring-type buildings. The hierarchical fuzzy comprehensive evaluation model is scientific and reasonable when used to measure the comprehensive benefits of carbon emissions from prefabricated buildings. By taking a project in Zhengzhou City, Henan Province as an example, the comprehensive evaluation results show that the carbon emissions of this project are at moderate levels. The carbon emissions from prefabricated buildings can be reduced by expanding the market scale of the building industry, adjusting its use of building materials, and setting up special funds for these buildings. The findings of this work provide a certain reference value for analysing the differences between prefabricated and traditional buildings in terms of their carbon emissions in the materialization phase, for evaluating how the carbon emissions of the former can be reduced, and for formulating and executing building emission reduction plans.

Natural microbial sensing circuits can be rewired into new gene networks to build living sensors that detect and respond to disease‐associated biomolecules. However, synthetic living sensors, once ingested, are cleared from the gastrointestinal (GI) tract within 48 h; retaining devices in the intestinal lumen is prone to intestinal blockage or device migration. To localize synthetic microbes and safely extend their residence in the GI tract for health monitoring and sustained drug release, an ingestible magnetic hydrogel carrier is developed to transport diagnostic microbes to specific intestinal sites. The magnetic living hydrogel is localized and retained by attaching a magnet to the abdominal skin, resisting the peristaltic waves in the intestine. The device retention is validated in a human intestinal phantom and an in vivo rodent model, showing that the ingestible hydrogel maintains the integrated living bacteria for up to seven days, which allows the detection of heme for GI bleeding in the harsh environment of the gut. The retention of microelectronics is also demonstrated by incorporating a temperature sensor into the magnetic hydrogel carrier. [ABSTRACT FROM AUTHOR]

Chimeric antigen receptor (CAR)-T cell therapies demonstrate the clinical potential of lymphocytes engineered with synthetic properties. However, CAR-T cells are ineffective in most solid tumors, partly due to inadequate activation of the infused lymphocytes at the site of malignancy. To selectively enhance antitumor efficacy without exacerbating off-target toxicities, CAR-T cells can be engineered to preferentially deliver immunostimulatory payloads in tumors. Here, we report a novel antigen-inducible promoter for conditional payload expression in primary human T cells. In therapeutic T cell models, the novel NR4A-based promoter induced higher reporter gene expression than the conventional NFAT-based promoter under weakly immunogenic conditions, where payload expression is most needed. Minimal activity was detected from the inducible promoters in the absence of antigen and after withdrawal of stimulation. As a functional proof-of-concept, we used the NR4A-based promoter to express cytokines in an antimesothelin CAR-T model with suboptimal stimulation and observed improved proliferation compared to T cells engineered with the conventional NFAT promoter or CAR alone. Our system achieves CAR-directed payload expression under weakly immunogenic conditions and could enable the next generation of cell therapies with enhanced antitumor efficacy.

Tumorigenesis is a complex process that is driven by a combination of networks of genes and environmental factors; however, efficient approaches to identifying functional networks that are perturbed by the process of tumorigenesis are lacking. In this study, we provide a comprehensive network-based strategy for the systematic discovery of functional synergistic modules that are causal determinants of inflammation-induced tumorigenesis. Our approach prioritizes candidate genes selected by integrating clinical-based and network-based genome-wide gene prediction methods and identifies functional synergistic modules based on combinatorial CRISPR-Cas9 screening. On the basis of candidate genes inferred de novo from experimental and computational methods to be involved in inflammation and cancer, we used an existing TGFβ1-induced cellular transformation model in colonic epithelial cells and a new combinatorial CRISPR-Cas9 screening strategy to construct an inflammation-induced differential genetic interaction network. The inflammation-induced differential genetic interaction network that we generated yielded functional insights into the genes and functional module combinations, and showed varied responses to the inflammation agents as well as active traditional Chinese medicine compounds. We identified opposing differential genetic interactions of inflammation-induced tumorigenesis: synergistic promotion and suppression. The synergistic promotion state was primarily caused by deletions in the immune and metabolism modules; the synergistic suppression state was primarily induced by deletions in the proliferation and immune modules or in the proliferation and metabolism modules. These results provide insight into possible early combinational targets and biomarkers for inflammation-induced tumorigenesis and highlight the synergistic effects that occur among immune, proliferation, and metabolism modules. In conclusion, this approach deepens the understanding of the underlying mechanisms that cause inflammation to potentially increase the cancer risk of colonic epithelial cells and accelerate the translation into novel functional modules or synergistic module combinations that modulate complex disease phenotypes.

Nuclease dead Cas9 (dCas9) has been widely used for modulating gene expression by fusing with different activation or repression domains. However, delivery of the CRISPR/Cas system fused with various effector domains in a single adeno-associated virus (AAV) remains challenging due to the payload limit. Here, we engineered a set of downsized variants of Cas9 including Staphylococcus aureus Cas9 (SaCas9) that retained DNA binding activity by deleting conserved functional domains. We demonstrated that fusing FokI nuclease domain to the N-terminal of the minimal SaCas9 (mini-SaCas9) or to the middle of the split mini-SaCas9 can trigger efficient DNA cleavage. In addition, we constructed a set of compact transactivation domains based on the tripartite VPR activation domain and self-assembled arrays of split SpyTag:SpyCatch peptides, which are suitable for fusing to the mini-SaCas9. Lastly, we produced a single AAV containing the mini-SaCas9 fused with a downsized transactivation domain along with an optimized gRNA expression cassette, which showed efficient transactivation activity. Our results highlighted a practical approach to generate down-sized CRISPR/Cas9 and gene activation systems for in vivo applications.