Experimental Demonstration of Stationary Dark-State Polaritons Dressed by Dipole-Dipole Interaction

Dark-state polaritons (DSPs) based on the effect of electromagnetically induced transparency are bosonic quasiparticles, representing the superpositions of photons and atomic ground-state coherences. It has been proposed that stationary DSPs are governed by the equation of motion closely similar to the Schr\"{o}dinger equation and can be employed to achieve Bose-Einstein condensation (BEC) with transition temperature orders of magnitude higher than that of the atomic BEC. The stationary-DSP BEC is a three-dimensional system and has a far longer lifetime than the exciton-polariton BEC. In this work, we experimentally demonstrated the stationary DSP dressed by the Rydberg-state dipole-dipole interaction (DDI). The DDI-induced phase shift of the stationary DSP was systematically studied. Notably, the experimental data are consistent with the theoretical predictions. The phase shift can be viewed as a consequence of elastic collisions. In terms of thermalization to achieve BEC, the $\mu$m$^2$-size interaction cross-section of the DDI can produce a sufficient elastic collision rate for the stationary DSPs. This work makes a substantial advancement toward the realization of the stationary-DSP BEC

Color-Octet Contributions to J/psi Photoproduction via Fragmentation at HERA

We study J/psi photoproduction via fragmentation at next-to-leading order in the QCD-improved parton model, using the nonrelativistic factorization formalism proposed by Bodwin, Braaten, and Lepage. We consider direct and resolved photoproduction of prompt J/psi mesons and chi_{cJ} mesons radiatively decaying to J/psi+gamma, taking into account the formation of both color-singlet and color-octet c anti-c states. Adopting the values of the long-distance color-octet matrix elements extracted from fits to prompt-J/psi data recently taken at the Fermilab Tevatron, we predict that measurements of J/psi photoproduction at DESY HERA should show a distinctive excess over the expectation based on the color-singlet model at small values of the inelasticity variable z. This is complementary to the expected enhancement at z close to 1 due to the color-octet contribution to photon-gluon fusion.Comment: 10 pages (Latex), 3 figures (Postscript

Reconstruction for Mandibular Implant Failure

Mandibular defects may result from tumor ablations, trauma, or radiation necrosis. Significant segmental mandibular loss or hemimandibular loss may sometimes be replaced with mandibular implants by ENT surgeons/oral surgeons/head and neck surgeons. However, this may bring about mandibular implant failure in long-term follow-up. Mandibular implant failures usually manifest as: soft tissue atrophy, mandibular implant extrusion, infection, facial nerve involvement, facial asymmetry, derangement of occlusion and mastication, orocutaneous fistula, etc. Over 30 years, the authors have treated 102 patients with mandibular implant failure. Reconstruction may involve removal of the mandibular implant and immediate replacement of the mandibular defect with a piece of vascularized bone flap, not only to compensate for bone loss but also to replace neighboring soft tissue and possible skin defects. Frequently used flaps have been vascularized iliac bone (89/102) or vascularized fibula grafts (13/102). During follow-up, iliac bone flap reconstruction has yielded more favorable results due to its ample bone bulk and adequate soft tissue coverage. Fibula flaps with osteotomies have been associated with an increasing incidence of malunion/nonunion and subsequent easy deformation

Enhancement of Canonical Wnt/β-Catenin Signaling Activity by HCV Core Protein Promotes Cell Growth of Hepatocellular Carcinoma Cells

BACKGROUND: The Hepatitis C virus (HCV) core protein has been implicated as a potential oncogene or a cofactor in HCV-related hepatocellular carcinoma (HCC), but the underlying mechanisms are unknown. Overactivation of the Wnt/β-catenin signaling is a major factor in oncogenesis of HCC. However, the pathogenesis of HCV core-associated Wnt/β-catenin activation remains to be further characterized. Therefore, we attempted to determine whether HCV core protein plays an important role in regulating Wnt/β-catenin signaling in HCC cells. METHODOLOGY: Wnt/β-catenin signaling activity was investigated in core-expressing hepatoma cells. Protein and gene expression were examined by Western blot, immunofluorescence staining, RT-qPCR, and reporter assay. PRINCIPAL FINDINGS: HCV core protein significantly enhances Tcf-dependent transcriptional activity induced by Wnt3A in HCC cell lines. Additionally, core protein increases and stabilizes β-catenin levels in hepatoma cell line Huh7 through inactivation of GSK-3β, which contributes to the up-regulation of downstream target genes, such as c-Myc, cyclin D1, WISP2 and CTGF. Also, core protein increases cell proliferation rate and promotes Wnt3A-induced tumor growth in the xenograft tumor model of human HCC. CONCLUSIONS/SIGNIFICANCE: HCV core protein enhances Wnt/β-catenin signaling activity, hence playing an important role in HCV-associated carcinogenesis

Directed and Elliptic Flow at RHIC

We present the directed flow measurement ($v_1$) from Au+Au collisions at \sqrtsNN = 62 GeV. Over the pseudorapidity range we have studied, which covers $\eta$ from -1.2 to 1.2 and $2.4 < |\eta| < 4$, the magnitude of $v_1$ for charged particles is found to increase monotonously with pseudorapidity for all centralities. No ``$v_1$ wiggle'', as predicted by various theoretical models, is observed at midrapidity. Elliptic flow ($v_2$) from moderate high $p_t$ particles ($3-6 GeV/c$) at \sqrtsNN = 200 GeV is presented as a function of impact parameter. It is found that models that are based on {\it jet quenching} alone appear to underpredict $v_2$ at moderate high $p_t$, while the model that incorporates both, recombination and fragmentation, describes the data better.Comment: 6 pages, 4 figures. Proceeding for Hot Quark 04 conference Changes in the revision are mostly English fixes. v1 versus eta plot is flipped over to follow the conventio

Assessment of hypermucoviscosity as a virulence factor for experimental Klebsiella pneumoniae infections: comparative virulence analysis with hypermucoviscosity-negative strain

<p>Abstract</p> <p>Background</p> <p><it>Klebsiella pneumoniae </it>displaying the hypermucoviscosity (HV) phenotype are considered more virulent than HV-negative strains. Nevertheless, the emergence of tissue-abscesses-associated HV-negative isolates motivated us to re-evaluate the role of HV-phenotype.</p> <p>Results</p> <p>Instead of genetically manipulating the HV-phenotype of <it>K. pneumoniae</it>, we selected two clinically isolated K1 strains, 1112 (HV-positive) and 1084 (HV-negative), to avoid possible interference from defects in the capsule. These well-encapsulated strains with similar genetic backgrounds were used for comparative analysis of bacterial virulence in a pneumoniae or a liver abscess model generated in either naïve or diabetic mice. In the pneumonia model, the HV-positive strain 1112 proliferated to higher loads in the lungs and blood of naïve mice, but was less prone to disseminate into the blood of diabetic mice compared to the HV-negative strain 1084. In the liver abscess model, 1084 was as potent as 1112 in inducing liver abscesses in both the naïve and diabetic mice. The 1084-infected diabetic mice were more inclined to develop bacteremia and had a higher mortality rate than those infected by 1112. A mini-Tn<it>5 </it>mutant of 1112, isolated due to its loss of HV-phenotype, was avirulent to mice.</p> <p>Conclusion</p> <p>These results indicate that the HV-phenotype is required for the virulence of the clinically isolated HV-positive strain 1112. The superior ability of the HV-negative stain 1084 over 1112 to cause bacteremia in diabetic mice suggests that factors other than the HV phenotype were required for the systemic dissemination of <it>K. pneumoniae </it>in an immunocompromised setting.</p

Cytochrome P450 Metabolism of Betel Quid-Derived Compounds: Implications for the Development of Prevention Strategies for Oral and Pharyngeal Cancers

Betel quid (BQ) products, with or without tobacco, have been classified by the International Agency for Research on Cancer (IARC) as group I human carcinogens that are associated with an elevated risk of oral potentially malignant disorders (OPMDs) and cancers of the oral cavity and pharynx. There are estimated 600 million BQ users worldwide. In Taiwan alone there are 2 million habitual users (approximately 10% of the population). Oral and pharyngeal cancers result from interactions between genes and environmental factors (BQ exposure). Cytochrome p450 (CYP) families are implicated in the metabolic activation of BQ- and areca nut-specific nitrosamines. In this review, we summarize the current knowledge base regarding CYP genetic variants and related oral disorders. In clinical applications, we focus on cancers of the oral cavity and pharynx and OPMDs associated with CYP gene polymorphisms, including CYP1A1, CYP2A6, CYP2E1, and CYP26B1. Our discussion of CYP polymorphisms provides insight into the importance of screening tests in OPMDs patients for the prevention of oral and pharyngeal cancers. Future studies will establish a strong foundation for the development of chemoprevention strategies, polymorphism-based clinical diagnostic tools (e.g., specific single-nucleotide polymorphism (SNP) “barcodes”), and effective treatments for BQ-related oral disorders

Osthole Stimulates Osteoblast Differentiation and Bone Formation by Activation of β-Catenin–BMP Signaling

Osteoporosis is defined as reduced bone mineral density with a high risk of fragile fracture. Current available treatment regimens include antiresorptive drugs such as estrogen receptor analogues and bisphosphates and anabolic agents such as parathyroid hormone (PTH). However, neither option is completely satisfactory because of adverse effects. It is thus highly desirable to identify novel anabolic agents to improve future osteoporosis treatment. Osthole, a coumarin-like derivative extracted from Chinese herbs, has been shown to stimulate osteoblast proliferation and differentiation, but its effect on bone formation in vivo and underlying mechanism remain unknown. In this study, we found that local injection of Osthole significantly increased new bone formation on the surface of mouse calvaria. Ovariectomy caused evident bone loss in rats, whereas Osthole largely prevented such loss, as shown by improved bone microarchitecture, histomorphometric parameters, and biomechanical properties. In vitro studies demonstrated that Osthole activated Wnt/β-catenin signaling, increased Bmp2 expression, and stimulated osteoblast differentiation. Targeted deletion of the β-catenin and Bmp2 genes abolished the stimulatory effect of Osthole on osteoblast differentiation. Since deletion of the Bmp2 gene did not affect Osthole-induced β-catenin expression and the deletion of the β-catenin gene inhibited Osthole-regulated Bmp2 expression in osteoblasts, we propose that Osthole acts through β-catenin–BMP signaling to promote osteoblast differentiation. Our findings demonstrate that Osthole could be a potential anabolic agent to stimulate bone formation and prevent estrogen deficiency–induced bone loss. © 2010 American Society for Bone and Mineral Research