Thermodynamics of spin-1/2 tetrameric Heisenberg antiferromagnetic chain

The thermodynamic properties of a spin S=1/2 tetrameric Heisenberg antiferromagnetic chain with alternating interactions AF1-AF2-AF1-F (AF and F denote the antiferromagnetic and ferromagnetic couplings, respectively) are studied by means of the transfer-matrix renormalization group method and Jordan-Wigner transformation. It is found that in the absence of magnetic field, the thermodynamic behaviors are closely related to the gapped low-lying excitations, and a novel structure with three peaks in the temperature dependence of specific heat is unveiled. In a magnetic field, a phase diagram in the temperature-field plane for the couplings satisfying JAF1=JAF2=JF is obtained, in which various phases are identified. The temperature dependence of thermodynamic quantities including the magnetization, susceptibility and specific heat are studied to characterize the corresponding phases. It is disclosed that the magnetization has a crossover behavior at low temperature in the Luttinger liquid phase, which is shown falling into the same class as that in the S=1 Haldane chain. In the plateau regime, the thermodynamic behaviors alter at a certain field, which results from the crossing of two excitation spectra. By means of the fermion mapping, it is uncovered that the system has four spectra from fermion and hole excitations that are responsible for the observed thermodynamic behaviors.Comment: 10 pages, 10 figures, accepted by Phys. Rev.

Hypoxia Exacerbates Inflammatory Acute Lung Injury via the Toll-Like Receptor 4 Signaling Pathway

Acute lung injury (ALI) is characterized by non-cardiogenic diffuse alveolar damage and often leads to a lethal consequence, particularly when hypoxia coexists. The treatment of ALI remains a challenge: pulmonary inflammation and hypoxia both contribute to its onset and progression and no effective prevention approach is available. Here, we aimed to investigate the underlying mechanism of hypoxia interaction with inflammation in ALI and to evaluate hypoxia-inducible factor 1 alpha (HIF-1α)—the crucial modulator in hypoxia—as a potential therapeutic target against ALI. First, we developed a novel ALI rat model induced by a combined low-dose of lipopolysaccharides (LPS) with acute hypoxia. Second, we used gene microarray analysis to evaluate the inflammatory profiles of bronchi alveolar lavage fluid cells of ALI rats. Third, we employed an alveolar macrophage cell line, NR8383 as an in vitro system together with a toll-like receptor 4 (TLR4) antagonist TAK-242, to verify our in vivo findings from ALI animals. Finally, we tested the therapeutic effects of HIF-1α augmentation against inflammation and hypoxia in ALI. We demonstrated that (i) LPS upregulated inflammatory genes, tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), in the alveolar macrophages of ALI rats, which were further enhanced when ALI combined with hypoxia; (ii) hypoxia exposure could further enhance the upregulation of alveolar macrophageal TLR4 that was noticed in LPS-induced inflammatory ALI, conversely, TLR4 antagonist TAK-242 could suppress the macrophageal expression of TLR4 and inflammatory cytokines, including TNF-α, IL-1β, and IL-6, suggesting that the TLR4 signaling pathway as a central link between inflammation and hypoxia in ALI; (iii) manipulation of HIF-1α in vitro could suppress TLR4 expression induced by combined LPS and hypoxia, via suppressing promoter activity of the TLR4 gene; (iv) preconditioning augmentation of HIF-1α in vivo by HIF hydroxylase inhibitor, DMOG excreted protection against inflammatory, and hypoxic processes in ALI. Together, we see that hypoxia can exacerbate inflammation in ALI via the activation of the TLR4 signaling pathway in alveolar macrophages and predispose impairment of the alveolar-capillary barrier in the development of ALI. Targeting HIF-1α can suppress TLR4 expression and macrophageal inflammation, suggesting the potential therapeutic and preventative value of HIF-1α/TLR4 crosstalk pathway in ALI

The Warming Acupuncture for Treatment of Sciatica in 30 Cases

ObjectiveTo observe the relation between the pain threshold and the therapeutic effects of acupuncture for sciatica.Methods90 sciatica patients were equally divided at random into the following 3 groups: a warming acupuncture group treated with the needles warmed by burning moxa, a western medicine group administered Nimesulide tablets and a point-injection group with Anisodamine injected. The pain threshold was tested before treatment and after the first, second and third treatment courses.ResultsThe warming acupuncture therapy showed better therapeutic effects than the other two groups with significant differences in the change of pain threshold and the improvement of clinical symptoms and signs (P < 0.01).ConclusionAcupuncture can relieve the symptoms of sciatica with the increase of pain threshold

Peripheral Leukocytapheresis Attenuates Acute Lung Injury Induced by Lipopolysaccharide In Vivo

The mortality of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) remains high and efforts for prevention and treatments have shown little improvement over the past decades. The present study investigated the efficacy and mechanism of leukocytapheresis (LCAP) to partially eliminate peripheral neutrophils and attenuate lipopolysaccharide (LPS)-induced lung injury in dogs. A total of 24 healthy male mongrel dogs were enrolled and randomly divided into LPS, LCAP and LCAP-sham groups. All animals were injected with LPS to induce endotoxemia. The serum levels of leucocytes, neutrophil elastase, arterial blood gas, nuclear factor-kappa B (NF-κB) subunit p65 in lung tissues were measured. The histopathology and parenchyma apoptosis of lung tissues were examined. We found that 7, 3, and 7 animals in the LPS, LCAP, and sham-LCAP groups, respectively, developed ALI 36 h after LPS infusion. The levels of NF-κB p65 in lung tissue, neutrophils and elastase in blood, decreased significantly following LCAP. LCAP also alleviated apoptosis, and NF-κB p65 in lung tissues. Collectively, our results show that partial removal of leucocytes from peripheral blood decreases elastase level in serum. This, in turn, attenuates lung injuries and may potentially decrease the incidence of ALI

The Anti-Inflammatory Activity of HMGB1 A Box Is Enhanced When Fused with C-Terminal Acidic Tail

HMGB1, composed of the A box, B box, and C tail domains, is a critical proinflammatory cytokine involved in diverse inflammatory diseases. The B box mediates proinflammatory activity, while the A box alone acts as a specific antagonist of HMGB1. The C tail contributes to the spatial structure of A box and regulates HMGB1 DNA binding specificity. It is unknown whether the C tail can enhance the anti-inflammatory effect of A box. In this study, we generated fusion proteins consisting of the A box and C tail, in which the B box was deleted and the A box and C tail were linked either directly or by the flexible linker sequence (Gly4Ser)3. In vitro and in vivo experiments showed that the two fusion proteins had a higher anti-inflammatory activity compared to the A box alone. This suggests that the fused C tail enhances the anti-inflammatory effect of the A box

Hg 0 capture over MoS2 nanosheets containing adsorbent: effects of temperature, space velocity, and other gas species

Fossil fuel burning is the largest anthropogenic source of mercury emission, which is expected to be the first industrial sector to be addressed under Minamata Convention. In this research, the preliminary investigation has been carried out to understand the effects of temperature, space velocity, and SO2 and O2 on Hg0 capture over MoS2 nanosheets containing elemental mercury adsorbent. The adsorbent exhibited excellent performance in the removal of Hg0 at a low temperature below 125°C (particularly at 50°C) with a space velocity below 9.0×104 ml/(h·g). It was found that the presence of O2 had positive effect on Hg0 removal whilst SO2 had slightly negative effect on mercury capture at low temperature, such as 50°C. However, such negative effect became negligible when O2 co-existed with SO2 in the simulated flue gas. The research provided fundamental information for further development of the 2D graphene-like MoS2 nanosheets containing adsorbent for mercury capture

USP10 is a potential mediator for vagus nerve stimulation to alleviate neuroinflammation in ischaemic stroke by inhibiting NF-κB signalling pathway

BackgroundVagus nerve stimulation (VNS) has a protective effect on neurological recovery in ischaemic stroke. However, its underlying mechanism remains to be clarified. Ubiquitin-specific protease 10 (USP10), a member of the ubiquitin-specific protease family, has been shown to inhibit the activation of the NF-κB signalling pathway. Therefore, this study investigated whether USP10 plays a key role in the protective effect of VNS against ischemic stroke and explore its mechanism.MethodsIschaemic stroke model was constructed by transient middle cerebral artery occlusion (tMCAO) in mice. VNS was performed at 30 min, 24hr, and 48hr after the establishment of tMCAO model. USP10 expression induced by VNS after tMCAO was measured. LV-shUSP10 was used to establish the model with low expression of USP10 by stereotaxic injection technique. The effects of VNS with or without USP10 silencing on neurological deficits, cerebral infarct volume, NF-κB pathway activation, glial cell activation, and release of pro-inflammation cytokines were assessed.ResultsVNS enhanced the expression of USP10 following tMCAO. VNS ameliorated neurological deficits and reduced cerebral infarct volume, but this effect was inhibited by silencing of USP10. Activation of the NF-κB pathway and the expression of inflammatory cytokines induced by tMCAO were suppressed by VNS. Moreover, VNS promoted the pro-to-anti-inflammatory response of microglia and inhibited activation of astrocytes, while silencing of USP10 prevented the neuroprotective and anti-neuroinflammatory effects of VNS.ConclusionUSP10 is a potential mediator for VNS to alleviate neurological deficits, neuroinflammation, and glial cell activation in ischaemic stroke by inhibiting NF-κB signalling pathway

Isospin dependence of projectile-like fragment production at intermediate energies

The cross sections of fragments produced in 140 $A$ MeV $^{40,48}$Ca + $^9$Be and $^{58,64}$Ni + $^9$Be reactions are calculated by the statistical abration-ablation(SAA) model and compared to the experimental results measured at the National Superconducting Cyclotron Laboratory (NSCL) at Michigan State University. The fragment isotopic and isotonic cross section distributions of $^{40}$Ca and $^{48}$Ca, $^{58}$Ni and $^{64}$Ni, $^{40}$Ca and $^{58}$Ni, and $^{48}$Ca and $^{64}$Ni are compared and the isospin dependence of the projectile fragmentation is studied. It is found that the isospin dependence decreases and disappears in the central collisions. The shapes of the fragment isotopic and isotonic cross section distributions are found to be very similar for symmetric projectile nuclei. The shapes of the fragment isotopic and isotonic distributions of different asymmetric projectiles produced in peripheral reactions are found very similar. The similarity of the distributions are related to the similar proton and neutron density distributions inside the nucleus in framework of the SAA model.Comment: 7 pages, 4 figures; to be published in Phys Rev

Scale-free download network for publications

The scale-free power-law behavior of the statistics of the download frequency of publications has been, for the first time, reported. The data of the download frequency of publications are taken from a well-constructed web page in the field of economic physics (http://www.unifr.ch/econophysics/). The Zipf-law analysis and the Tsallis entropy method were used to fit the download frequency. It was found that the power-law exponent of rank-ordered frequency distribution is $\gamma \sim 0.38 \pm 0.04$ which is consistent with the power-law exponent $\alpha \sim 3.37 \pm 0.45$ for the cumulated frequency distributions. Preferential attachment model of Barabasi and Albert network has been used to explain the download network.Comment: 3 pages, 2 figure