Holographic Techni-dilaton

Techni-dilaton, a pseudo-Nambu-Goldstone boson of scale symmetry, was predicted long ago in the Scale-invariant/Walking/Conformal Technicolor (SWC-TC) as a remnant of the (approximate) scale symmetry associated with the conformal fixed point, based on the conformal gauge dynamics of ladder Schwinger-Dyson (SD) equation with non-running coupling. We study the techni-dilaton as a flavor-singlet bound state of techni-fermions by including the techni-gluon condensate (tGC) effect into the previous (bottom-up) holographic approach to the SWC-TC, a deformation of the holographic QCD with $\gamma_m \simeq 0$ by large anomalous dimension $\gamma_m \simeq 1$. With including a bulk scalar field corresponding to the gluon condensate, we first improve the Operator Product Expansion of the current correlators so as to reproduce gluonic $1/Q^4$ term both in QCD and SWC-TC. We find in QCD about $10\%$ (negative) contribution of gluon condensate to the $\rho$ meson mass. We also calculate the oblique electroweak $S$-parameter in the presence of the effect of the tGC and find that for the fixed value of $S$ the tGC effects dramatically reduce the flavor-singlet scalar (techni-dilaton) mass $M_{\rm TD}$ (in the unit of $F_\pi$), while the vector and axial-vector masses $M_\rho$ and $M_{a_1}$ are rather insensitive to the tGC, where $F_\pi$ is the decay constant of the techni-pion. If we use the range of values of tGC implied by the ladder SD analysis of the non-perturbative scale anomaly in the large $N_f$ QCD near the conformal window, the phenomenological constraint $S \simeq 0.1$ predicts the techni-dilaton mass $M_{\rm TD} \sim 600$ GeV which is within reach of LHC discovery.Comment: 28 pages, 11 eps files, typos corrected, references added, Fig.1 corrected, some discussions added, to be published in PR

Techni-dilaton at Conformal Edge

Techni-dilaton (TD) was proposed long ago in the technicolor (TC) near criticality/conformality. To reveal the critical behavior of TD, we explicitly compute the nonperturbative contributions to the scale anomaly $$and to the techni-gluon condensate$$, which are generated by the dynamical mass m of the techni-fermions. Our computation is based on the (improved) ladder Schwinger-Dyson equation, with the gauge coupling $\alpha$ replaced by the two-loop running one $\alpha(\mu)$ having the Caswell-Banks-Zaks IR fixed point $\alpha_*$: $\alpha(\mu) \simeq \alpha = \alpha_*$ for the IR region $m < \mu < \Lambda_{TC}$, where $\Lambda_{TC}$ is the intrinsic scale (analogue of $\Lambda_{QCD}$ of QCD) relevant to the perturbative scale anomaly. We find that $-/m^4\to const \ne 0$ and $/m^4\to (\alpha/\alpha_{cr}-1)^{-3/2}\to\infty$ in the criticality limit $m/\Lambda_{TC}\sim\exp(-\pi/(\alpha/\alpha_{cr}-1)^{1/2})\to 0$ ($\alpha=\alpha_* \to \alpha_{cr}$) ("conformal edge"). Our result precisely reproduces the formal identity $=(\beta(\alpha)/4 \alpha)$, where $\beta(\alpha)=-(2\alpha_{cr}/\pi) (\alpha/\alpha_{cr}-1)^{3/2}$ is the nonperturbative beta function corresponding to the above essential singularity scaling of $m/\Lambda_{TC}$. Accordingly, the PCDC implies $(M_{TD}/m)^2 (F_{TD}/m)^2=-4/m^4 \to const \ne 0$ at criticality limit, where $M_{TD}$ is the mass of TD and $F_{TD}$ the decay constant of TD. We thus conclude that at criticality limit the TD could become a "true (massless) Nambu-Goldstone boson" $M_{TD}/m\to 0$, only when $m/F_{TD}\to 0$, namely getting decoupled, as was the case of "holographic TD" of Haba-Matsuzaki-Yamawaki. The decoupled TD can be a candidate of dark matter.Comment: 17 pages, 14 figures; discussions clarified, references added, to appear in Phys.Rev.

DNA demethylation-dependent enhancement of toll-like receptor-2 gene expression in cystic fibrosis epithelial cells involves SP1-activated transcription

<p>Abstract</p> <p>Background</p> <p>The clinical course of cystic fibrosis (CF) is characterized by recurrent pulmonary infections and chronic inflammation. We have recently shown that decreased methylation of the toll-like receptor-2 (TLR2) promoter leads to an apparent CF-related up-regulation of TLR2. This up-regulation could be responsible, in part, for the CF-associated enhanced proinflammatory responses to various bacterial products in epithelial cells. However, the molecular mechanisms underlying DNA hypomethylation-dependent enhancement of TLR2 expression in CF cells remain unknown.</p> <p>Results</p> <p>The present study indicates that there is a specific CpG region (CpG#18-20), adjacent to the SP1 binding site that is significantly hypomethylated in several CF epithelial cell lines. These CpGs encompass a minimal promoter region required for basal TLR2 expression, and suggests that CpG#18-20 methylation regulates TLR2 expression in epithelial cells. Furthermore, reporter gene analysis indicated that the SP1 binding site is involved in the methylation-dependent regulation of the TLR2 promoter. Inhibition of SP1 with mithramycin A decreased TLR2 expression in both CF and 5-azacytidine-treated non-CF epithelial cells. Moreover, even though SP1 binding was not affected by CpG methylation, SP1-dependent transcription was abolished by CpG methylation.</p> <p>Conclusion</p> <p>This report implicates SP1 as a critical component of DNA demethylation-dependent up-regulation of TLR2 expression in CF epithelial cells.</p

Carbonization and H3PO4 activation of fern Dicranopteris linearis and electrochemical properties for electric double layer capacitor electrode

Today, the world’s climate change is a growing problem, plant carbon sequestration is one of the effective ways to mitigate climate change by reducing greenhouse gases, mostly carbon gases. Dicranopteris linearis (D. linearis), a common fern species in the tropic or subtropic ecoregions, has been recently recognized as a potential feedstock to produce highly porous biochar. This study aims to enhance the specific surface area (SSA) and pore volumes of biochars derived from the D. linearis by H3PO4 activation and examine electrical properties of the activated biochars and their possible usage for the electric double-layer capacitor (EDLC) electrode. The treated raw fern was activated with H3PO4 85% by the three different mixing ratios 1:0, 1:1, and 1:3 (w/w) and then pyrolysis under N2 flow maintained at 500 °C for 1 h. The performance as the electrode for an EDLC was evaluated in 1 mol L−1 H2SO4 solution for the H3PO4-activated samples. The SSA and pore volumes were drastically increased after activation. The maximum SSA and pore volume were 1212 m2 g−1 and 1.43 cm3 g−1, respectively for the biochar activated at 400 °C with a weight mixing ratio 1:3 (w/w) between the fern and H3PO4 acid while these values of the biochar at 400 °C were 12 m2 g−1 and 0.02 cm3 g−1, respectively. The biochar activated at 600 °C with the mixing ratio 1:1 (w/w) showed the maximum capacitance value, ca. 108 F g−1 at 1 mV s−1. The activation using H3PO4 showed a positive tendency to enhance electrochemical properties and it could be a premise toward a higher performance of EDLC from the D. linearis derived activated biochar

Zinc Deficiency via a Splice Switch in Zinc Importer ZIP2/SLC39A2 Causes Cystic Fibrosis-Associated MUC5AC Hypersecretion in Airway Epithelial Cells

Airway mucus hyperproduction and fluid imbalance are important hallmarks of cystic fibrosis (CF), the most common life-shortening genetic disorder in Caucasians. Dysregulated expression and/or function of airway ion transporters, including cystic fibrosis transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC), have been implicated as causes of CF-associated mucus hypersecretory phenotype. However, the contributory roles of other substances and transporters in the regulation of CF airway pathogenesis remain unelucidated. Here, we identified a novel connection between CFTR/ENaC expression and the intracellular Zn2 + concentration in the regulation of MUC5AC, a major secreted mucin that is highly expressed in CF airway. CFTR-defective and ENaC-hyperactive airway epithelial cells specifically and highly expressed a unique, alternative splice isoform of the zinc importer ZIP2/SLC39A2 (ΔC-ZIP2), which lacks the C-terminal domain. Importantly, ΔC-ZIP2 levels correlated inversely with wild-type ZIP2 and intracellular Zn2 + levels. Moreover, the splice switch to ΔC-ZIP2 as well as decreased expression of other ZIPs caused zinc deficiency, which is sufficient for induction of MUC5AC; while ΔC-ZIP2 expression per se induced ENaC expression and function. Thus, our findings demonstrate that the novel splicing switch contributes to CF lung pathology via the novel interplay of CFTR, ENaC, and ZIP2 transporters

Collagenous Fibroma (Desmoplastic Fibroblastoma) of the Neck Presenting with Neurological Symptoms

Collagenous fibromas are rare fibrous soft tissue tumours that usually arise in subcutaneous tissue or skeletal muscle at a variety of anatomical sites. These lesions commonly present as painless, slow-growing mobile masses. We describe a unique case of a 41-year-old woman presenting with a posterior neck swelling and longstanding history of severe ongoing pain in the right scapular region, shoulder and neck, weakness of the palmar grip and limited right lateral neck flexion and rotation. A history of trauma to the right neck in adolescence was noted. Histological analysis revealed a paucicellular lesion with spindle and stellate-shaped fibroblasts involving the cervical nerve roots, typical of collagenous fibroma. In a literature search on Medline and Pubmed, we found no reported cases of collagenous fibromas presenting with neurological symptoms. This report highlights the potential of these lesions to present with neurological symptoms due to infiltration of surrounding tissues, and that preceding trauma may contribute to the aetiology

Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis

BACKGROUND: Toll-like receptors enable the host to recognize a large number of pathogen-associated molecular patterns such as bacterial lipopolysaccharide, viral RNA, CpG-containing DNA and flagellin. Toll-like receptors have also been shown to play a pivotal role in both innate and adaptive immune responses. The role of Toll-like receptors as a primary part of our microbe defense system has been shown in several studies, but their possible function as mediators in allergy and asthma remains to be established. The present study was designed to examine the expression of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with intermittent allergic rhinitis, focusing on changes induced by exposure to pollen. METHODS: 27 healthy controls and 42 patients with seasonal allergic rhinitis volunteered for the study. Nasal biopsies were obtained before and during pollen season as well as before and after allergen challenge. The seasonal material was used for mRNA quantification of Toll-like receptors 2, 3 and 4 with real-time polymerase chain reaction, whereas specimens achieved in conjunction with allergen challenge were used for immunohistochemical localization and quantification of corresponding proteins. RESULTS: mRNA and protein representing Toll-like receptors 2, 3 and 4 could be demonstrated in all specimens. An increase in protein expression for all three receptors could be seen following allergen challenge, whereas a significant increase of mRNA only could be obtained for Toll-like receptor 3 during pollen season. CONCLUSION: The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation