Graded reflection equation algebras and integrable Kondo impurities in the one-dimensional t-J model

Integrable Kondo impurities in two cases of the one-dimensional $t-J$ model are studied by means of the boundary ${\bf Z}_2$-graded quantum inverse scattering method. The boundary $K$ matrices depending on the local magnetic moments of the impurities are presented as nontrivial realizations of the reflection equation algebras in an impurity Hilbert space. Furthermore, these models are solved by using the algebraic Bethe ansatz method and the Bethe ansatz equations are obtained.Comment: 14 pages, RevTe

Application of Instantons: Quenching of Macroscopic Quantum Coherence and Macroscopic Fermi-Particle Configurations

Starting from the coherent state representation of the evolution operator with the help of the path-integral, we derive a formula for the low-lying levels $E = \epsilon_0 - 2\triangle\epsilon cos (s+\xi)\pi$ of a quantum spin system. The quenching of macroscopic quantum coherence is understood as the vanishing of $cos (s+\xi)\pi$ in disagreement with the suppression of tunneling (i.e. $\triangle\epsilon = 0$) as claimed in the literature. A new configuration called the macroscopic Fermi-particle is suggested by the character of its wave function. The tunneling rate ($(2\triangle\epsilon)/(\pi)$) does not vanish, not for integer spin s nor for a half-integer value of s, and is calculated explicitly (for the position dependent mass) up to the one-loop approximation.Comment: 13 pages, LaTex, no figure

Ozone Inhalation Attenuated the Effects of Budesonide on Aspergillus fumigatus-Induced Airway Inflammation and Hyperreactivity in Mice.

Inhaled glucocorticoids form the mainstay of asthma treatment because of their anti-inflammatory effects in the lung. Exposure to the air pollutant ozone (O3) exacerbates chronic airways disease. We and others showed that presence of the epithelial-derived surfactant protein-D (SP-D) is important in immunoprotection against inflammatory changes including those induced by O3 inhalation in the airways. SP-D synthesis requires glucocorticoids. We hypothesized here that O3 exposure impairs glucocorticoid responsiveness (including SP-D production) in allergic airway inflammation. The effects of O3 inhalation and glucocorticoid treatment were studied in a mouse model of allergic asthma induced by sensitization and challenge with Aspergillus fumigatus (Af) in vivo. The role of O3 and glucocorticoids in regulation of SP-D expression was investigated in A549 and primary human type II alveolar epithelial cells in vitro. Budesonide inhibited airway hyperreactivity, eosinophil counts in the lung and bronchoalveolar lavage (BAL) and CCL11, IL-13, and IL-23p19 release in the BAL of mice sensitized and challenged with Af (p < 0.05). The inhibitory effects of budesonide were attenuated on inflammatory changes and were completely abolished on airway hyperreactivity after O3 exposure of mice sensitized and challenged with Af. O3 stimulated release of pro-neutrophilic mediators including CCL20 and IL-6 into the airways and impaired the inhibitory effects of budesonide on CCL11, IL-13 and IL-23. O3 also prevented budesonide-induced release of the immunoprotective lung collectin SP-D into the airways of allergen-challenged mice. O3 had a bi-phasic direct effect with early (<12 h) inhibition and late (>48 h) activation of SP-D mRNA (sftpd) in vitro. Dexamethasone and budesonide induced sftpd transcription and translation in human type II alveolar epithelial cells in a glucocorticoid receptor and STAT3 (an IL-6 responsive transcription factor) dependent manner. Our study indicates that O3 exposure counteracts the effects of budesonide on airway inflammation, airway hyperreactivity, and SP-D production. We speculate that impairment of SP-D expression may contribute to the acute O3-induced airway inflammation. Asthmatics exposed to high ambient O3 levels may become less responsive to glucocorticoid treatment during acute exacerbations

Geoarchaeological evidence of the AD 1642 Yellow River flood that destroyed Kaifeng, a former capital of dynastic China

Rising global temperatures will increase the number of extreme weather events, creating new challenges for cities around the world. Archaeological research on the destruction and subsequent reoccupation of ancient cities has the potential to reveal geological and social dynamics that have historically contributed to making urban settings resilient to these extreme weather events. Using a combination of archaeological and geological methods, we examine how extreme flood events at Kaifeng, a former capital of dynastic China, have shaped the city’s urban resilience. Specifically, we focus on an extreme Yellow River flood event in AD 1642 that historical records suggest killed around 300,000 people living in Kaifeng. Our recent archaeological excavations have discovered compelling geological and archaeological evidence that corroborates these documents, revealing that the AD 1642 Yellow River flood destroyed Kaifeng’s inner city, entombing the city and its inhabitants within meters of silt and clay. We argue that the AD 1642 flood was extraordinarily catastrophic because Kaifeng’s city walls only partly collapsed, entrapping most of the flood waters within the city. Both the geology of the Yellow River floods as well as the socio-political context of Kaifeng shaped the city’s resilience to extreme flood events