370 research outputs found

    Formulation of the Spinor Field in the Presence of a Minimal Length Based on the Quesne-Tkachuk Algebra

    Full text link
    In 2006 Quesne and Tkachuk (J. Phys. A: Math. Gen. {\bf 39}, 10909, 2006) introduced a (D+1)-dimensional (β,β)(\beta,\beta')-two-parameter Lorentz-covariant deformed algebra which leads to a nonzero minimal length. In this work, the Lagrangian formulation of the spinor field in a (3+1)-dimensional space-time described by Quesne-Tkachuk Lorentz-covariant deformed algebra is studied in the case where β=2β\beta'=2\beta up to first order over deformation parameter β\beta. It is shown that the modified Dirac equation which contains higher order derivative of the wave function describes two massive particles with different masses. We show that physically acceptable mass states can only exist for β<18m2c2\beta<\frac{1}{8m^{2}c^{2}}. Applying the condition β<18m2c2\beta<\frac{1}{8m^{2}c^{2}} to an electron, the upper bound for the isotropic minimal length becomes about 3×1013m3 \times 10^{-13}m. This value is near to the reduced Compton wavelength of the electron (λc=mec=3.86×1013m)(\lambda_c = \frac{\hbar}{m_{e}c} = 3.86\times 10^{-13} m) and is not incompatible with the results obtained for the minimal length in previous investigations.Comment: 11 pages, no figur

    Formulation of an Electrostatic Field with a Charge Density in the Presence of a Minimal Length Based on the Kempf Algebra

    Full text link
    In a series of papers, Kempf and co-workers (J. Phys. A: Math. Gen. {\bf 30}, 2093, (1997); Phys. Rev. D {\bf52}, 1108, (1995); Phys. Rev. D {\bf55}, 7909, (1997)) introduced a D-dimensional (β,β)(\beta,\beta')-two-parameter deformed Heisenberg algebra which leads to a nonzero minimal observable length. In this work, the Lagrangian formulation of an electrostatic field in three spatial dimensions described by Kempf algebra is studied in the case where β=2β\beta'=2\beta up to first order over deformation parameter β\beta. It is shown that there is a similarity between electrostatics in the presence of a minimal length (modified electrostatics) and higher derivative Podolsky's electrostatics. The important property of this modified electrostatics is that the classical self-energy of a point charge becomes a finite value. Two different upper bounds on the isotropic minimal length of this modified electrostatics are estimated. The first upper bound will be found by treating the modified electrostatics as a classical electromagnetic system, while the second one will be estimated by considering the modified electrostatics as a quantum field theoretic model. It should be noted that the quantum upper bound on the isotropic minimal length in this paper is near to the electroweak length scale (electroweak1018m)(\ell_{electroweak}\sim 10^{-18}\, m).Comment: 11 pages, no figur

    Transdifferentiation of Human Dental Pulp Stem Cells Into Oligoprogenitor Cells

    Get PDF
    Introduction: The nerve fibers in central nervous system are surrounded by myelin sheet which is formed by oligodendrocytes. Cell therapy based on oligodendrocytes and their precursors transplantation can hold a promising alternative treatment for myelin sheet repair in demyelinating diseases. Methods: Human Dental Pulp Stem Cells (hDPSCs) are noninvasive, autologous and easy available source with multipotency characteristics, so they are in focus of interest in regenerative medicine. In the present study, hDPSCs were differentiated into oligoprogenitor using glial induction media, containing Retinoic Acid (RA), basic Fibroblast Growth Factor (bFGF), Platelet- Derived Growth Factor (PDGF), N2 and B27. The differentiated Oligoprogenitor Cells (OPCs) were evaluated for nestin, Olig2, NG2 and O4 using immunocytochemistry. Also, the expression of nestin, Olig2 and PDGFR-alpha gens (neuroprogenitor and oligoprogenitor markers) were investigated via RT-PCR technique. Results: The results indicate that glial differentiation medium induces the generation of oligoprogenitor cells as revealed via exhibition of specific glial markers, including Olig2, NG2 and O4. The expersion of nestin gene (neuroprogenitor marker) and Olig2 and PDGFR-alpha genes (oligoprogentor markers) were detected in treated hDPSCs at the end of the induction stage. Conclusion: hDPSCs can be induced to transdifferentiate into oligoprogenitor cells and respond to the routinely applied regents for glial differentiation of mesanchymal stem cells. These data suggest the hDPSCs as a valuable source for cell therapy in neurodegenerative diseases

    Novel weight functions and stress intensity factors for quarterelliptical cracks in lug attachments

    Get PDF
    In this paper, a general weight function was developed to calculate the stress intensity factors (SIFs) for quarter-elliptical cracks in a wide range of lug attachment family. For this purpose, a series of finite element analyses were conducted to achieve this weight function. Finally, using this unique extracted weight function, the influence of the pin loading model and crack parameters (aspect ratio and relative depth of the quarter-elliptical crack) on the SIFs was evaluated in the cracked lug attachments. The results of the present work were compared with those in the literature, which are compatible with them in those cases

    Inflammasome Sensor Nlrp1b-Dependent Resistance to Anthrax Is Mediated by Caspase-1, IL-1 Signaling and Neutrophil Recruitment

    Get PDF
    Bacillus anthracis infects hosts as a spore, germinates, and disseminates in its vegetative form. Production of anthrax lethal and edema toxins following bacterial outgrowth results in host death. Macrophages of inbred mouse strains are either sensitive or resistant to lethal toxin depending on whether they express the lethal toxin responsive or non-responsive alleles of the inflammasome sensor Nlrp1b (Nlrp1bS/S or Nlrp1bR/R, respectively). In this study, Nlrp1b was shown to affect mouse susceptibility to infection. Inbred and congenic mice harboring macrophage-sensitizing Nlrp1bS/S alleles (which allow activation of caspase-1 and IL-1β release in response to anthrax lethal toxin challenge) effectively controlled bacterial growth and dissemination when compared to mice having Nlrp1bR/R alleles (which cannot activate caspase-1 in response to toxin). Nlrp1bS-mediated resistance to infection was not dependent on the route of infection and was observed when bacteria were introduced by either subcutaneous or intravenous routes. Resistance did not occur through alterations in spore germination, as vegetative bacteria were also killed in Nlrp1bS/S mice. Resistance to infection required the actions of both caspase-1 and IL-1β as Nlrp1bS/S mice deleted of caspase-1 or the IL-1 receptor, or treated with the Il-1 receptor antagonist anakinra, were sensitized to infection. Comparison of circulating neutrophil levels and IL-1β responses in Nlrp1bS/S,Nlrp1bR/R and IL-1 receptor knockout mice implicated Nlrp1b and IL-1 signaling in control of neutrophil responses to anthrax infection. Neutrophil depletion experiments verified the importance of this cell type in resistance to B. anthracis infection. These data confirm an inverse relationship between murine macrophage sensitivity to lethal toxin and mouse susceptibility to spore infection, and establish roles for Nlrp1bS, caspase-1, and IL-1β in countering anthrax infection

    Adenoviral expression of a bispecific VHH-based neutralizing agent that targets protective antigen provides prophylactic protection from anthrax in mice

    Get PDF
    Bacillus anthracis, the causative agent of anthrax, secretes three polypeptides, which form the bipartite lethal and edema toxins (LT and ET, respectively). The common component in these toxins, protective antigen (PA), is responsible for binding to cellular receptors and translocating the lethal factor (LF) and edema factor (EF) enzymatic moieties to the cytosol. Antibodies against PA protect against anthrax. We previously isolated toxin-neutralizing variable domains of camelid heavy-chain-only antibodies (VHHs) and demonstrated their in vivo efficacy. In this work, gene therapy with an adenoviral (Ad) vector (Ad/VNA2-PA) (VNA, VHH-based neutralizing agents) promoting the expression of a bispecific VHH-based neutralizing agent (VNA2-PA), consisting of two linked VHHs targeting different PA-neutralizing epitopes, was tested in two inbred mouse strains, BALB/cJ and C57BL/6J, and found to protect mice against anthrax toxin challenge and anthrax spore infection. Two weeks after a single treatment with Ad/VNA2-PA, serum VNA2-PA levels remained above 1 μg/ml, with some as high as 10 mg/ml. The levels were 10- to 100-fold higher and persisted longer in C57BL/6J than in BALB/cJ mice. Mice were challenged with a lethal dose of LT or spores at various times after Ad/VNA2-PA administration. The majority of BALB/cJ mice having serum VNA2-PA levels of >0.1 μg/ml survived LT challenge, and 9 of 10 C57BL/6J mice with serum levels of >1 μg/ml survived spore challenge. Our findings demonstrate the potential for genetic delivery of VNAs as an effective method for providing prophylactic protection from anthrax. We also extend prior findings of mouse strain-based differences in transgene expression and persistence by adenoviral vectors

    Anthrax Lethal Toxin Suppresses Murine Cardiomyocyte Contractile Function and Intracellular Ca2+ Handling via a NADPH Oxidase-Dependent Mechanism

    Get PDF
    OBJECTIVES: Anthrax infection is associated with devastating cardiovascular sequelae, suggesting unfavorable cardiovascular effects of toxins originated from Bacillus anthracis namely lethal and edema toxins. This study was designed to examine the direct effect of lethal toxins on cardiomyocyte contractile and intracellular Ca(2+) properties. METHODS: Murine cardiomyocyte contractile function and intracellular Ca(2+) handling were evaluated including peak shortening (PS), maximal velocity of shortening/ relengthening (± dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR(90)), intracellular Ca(2+) rise measured as fura-2 fluorescent intensity (ΔFFI), and intracellular Ca(2+) decay rate. Stress signaling and Ca(2+) regulatory proteins were assessed using Western blot analysis. RESULTS: In vitro exposure to a lethal toxin (0.05-50 nM) elicited a concentration-dependent depression on cardiomyocyte contractile and intracellular Ca(2+) properties (PS, ± dL/dt, ΔFFI), along with prolonged duration of contraction and intracellular Ca(2+) decay, the effects of which were nullified by the NADPH oxidase inhibitor apocynin. The lethal toxin significantly enhanced superoxide production and cell death, which were reversed by apocynin. In vivo lethal toxin exposure exerted similar time-dependent cardiomyocyte mechanical and intracellular Ca(2+) responses. Stress signaling cascades including MEK1/2, p38, ERK and JNK were unaffected by in vitro lethal toxins whereas they were significantly altered by in vivo lethal toxins. Ca(2+) regulatory proteins SERCA2a and phospholamban were also differentially regulated by in vitro and in vivo lethal toxins. Autophagy was drastically triggered although ER stress was minimally affected following lethal toxin exposure. CONCLUSIONS: Our findings indicate that lethal toxins directly compromised murine cardiomyocyte contractile function and intracellular Ca(2+) through a NADPH oxidase-dependent mechanism
    corecore