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

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 $(\beta,\beta')$-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 $\beta'=2\beta$ up to first order over deformation parameter $\beta$. 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 $(\ell_{electroweak}\sim 10^{-18}\, m)$.Comment: 11 pages, no figur

The effect of interaguild predation on avoidance behavior of the aphidophagous midge, Aphidoletes aphidimyza (Dip.: Cecidomyiidae) on its encounter with the predatory bug Orius laevigatus (Het.: Anthocoridae)

The predatory bug, Orius laevigatus (Fibber), and the predatory midge, Aphidoletes aphidimyza Rondani, belong to an aphidophagous guild, feeding on the cotton aphid Aphis gossypii Glover. In this study some avoidance behavior of the predatory midge such as dropping from the plant and choosing an oviposition site in the face of interaguild (IG) predator O. laevigatus are investigated. The results indicate that A. aphidimyza females prefer not to lay eggs when they discover that their offspring would be at risk of being attacked by the IG predator. The experiment also shows that the dropping behavior of predatory midge larva, upon being spotted by the predatory bug (44.5%), is significantly higher than the control (6.5%). Both the dropping behavior and mortality of IG prey are found to be influenced by all developmental stages of the cotton aphid. The percentage of mortality and dropping rates of A. aphidimyza larvae in the presence of 2nd instar nymphs of aphids were 10% and 12.5% and for 4th instar nymphs were 31% and 44.5%, respectively. These findings confirm the correlation between habitat choice of A. aphidimyza, in relation to predation risk for its offspring, and also underscore the population structure of prey for avoidance behavior strategy of the aphidophagous midge in an interaguild predation system

Fitness costs of cornicle secretions as a defense mechanism for cotton aphid, Aphis gossypii (Hem.: Aphididae)

The cornicle secretion is a defensive mechanism in many aphid species to warn the related individuals of predation by natural enemies. Many researches have been conducted on the benefits of cornicle droplet and alarm pheromone but the cost of this phenomenon is poorly investigated. This study is intended to evaluate the direct fitness cost of cornicle secretion of immature as well as mature cotton aphids, Aphis gossypii Glover. Aphids were artificially forced to produce cornicle droplets at different stages of their development (second, third and fourth instars as well as adults). They were lightly stroked on the anterior portion of the thorax with a fine brush, resulting in the secretion of visible cornicle droplets. After this manipulation, life-history parameters of aphids were recorded until the death of the last adult individual. Experiments were conducted in a growth chamber at 25 ± 1°C, 50 ± 5% RH and a photoperiod of 16 L: 8 D hours. The results showed that the secretion of cornicle droplets by second and third instar nymphs of cotton aphid did not affect their survivorship and the number of offspring produced by their adult stage. In contrast, fourth instar nymphs as well as adults that emitted cornicle droplets had significantly lower survivorship and offspring production than non-secretors. The cornicle secretion has also fitness costs on the late instar and adult cotton aphids

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

In 2006 Quesne and Tkachuk (J. Phys. A: Math. Gen. {\bf 39}, 10909, 2006) introduced a (D+1)-dimensional $(\beta,\beta')$-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 $\beta'=2\beta$ up to first order over deformation parameter $\beta$. 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 $\beta<\frac{1}{8m^{2}c^{2}}$. Applying the condition $\beta<\frac{1}{8m^{2}c^{2}}$ to an electron, the upper bound for the isotropic minimal length becomes about $3 \times 10^{-13}m$. This value is near to the reduced Compton wavelength of the electron $(\lambda_c = \frac{\hbar}{m_{e}c} = 3.86\times 10^{-13} m)$ and is not incompatible with the results obtained for the minimal length in previous investigations.Comment: 11 pages, no figur

Transdifferentiation of Human Dental Pulp Stem Cells Into Oligoprogenitor Cells

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

Quantum Gravitational Corrections to the Real Klein-Gordon Field in the Presence of a Minimal Length

The (D+1)-dimensional $(\beta,\beta')$-two-parameter Lorentz-covariant deformed algebra introduced by Quesne and Tkachuk [C. Quesne and V. M. Tkachuk, J. Phys. A: Math. Gen. \textbf {39}, 10909 (2006).], leads to a nonzero minimal uncertainty in position (minimal length). The Klein-Gordon equation in a (3+1)-dimensional space-time described by Quesne-Tkachuk Lorentz-covariant deformed algebra is studied in the case where $\beta'=2\beta$ up to first order over deformation parameter $\beta$. It is shown that the modified Klein-Gordon equation which contains fourth-order derivative of the wave function describes two massive particles with different masses. We have shown that physically acceptable mass states can only exist for $\beta<\frac{1}{8m^{2}c^{2}}$ which leads to an isotropic minimal length in the interval $10^{-17}m<(\bigtriangleup X^{i})_{0}<10^{-15}m$. Finally, we have shown that the above estimation of minimal length is in good agreement with the results obtained in previous investigations.Comment: 10 pages, no figur

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

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

Anthrax Lethal Toxin Disrupts Intestinal Barrier Function and Causes Systemic Infections with Enteric Bacteria

A variety of intestinal pathogens have virulence factors that target mitogen activated protein kinase (MAPK) signaling pathways, including Bacillus anthracis. Anthrax lethal toxin (LT) has specific proteolytic activity against the upstream regulators of MAPKs, the MAPK kinases (MKKs). Using a murine model of intoxication, we show that LT causes the dose-dependent disruption of intestinal epithelial integrity, characterized by mucosal erosion, ulceration, and bleeding. This pathology correlates with an LT-dependent blockade of intestinal crypt cell proliferation, accompanied by marked apoptosis in the villus tips. C57BL/6J mice treated with intravenous LT nearly uniformly develop systemic infections with commensal enteric organisms within 72 hours of administration. LT-dependent intestinal pathology depends upon its proteolytic activity and is partially attenuated by co-administration of broad spectrum antibiotics, indicating that it is both a cause and an effect of infection. These findings indicate that targeting of MAPK signaling pathways by anthrax LT compromises the structural integrity of the mucosal layer, serving to undermine the effectiveness of the intestinal barrier. Combined with the well-described immunosuppressive effects of LT, this disruption of the intestinal barrier provides a potential mechanism for host invasion via the enteric route, a common portal of entry during the natural infection cycle of Bacillus anthracis

Anthrax Toxins Induce Shock in Rats by Depressed Cardiac Ventricular Function

Anthrax infections are frequently associated with severe and often irreversible hypotensive shock. The isolated toxic proteins of Bacillus anthracis produce a non-cytokine-mediated hypotension in rats by unknown mechanisms. These observations suggest the anthrax toxins have direct cardiovascular effects. Here, we characterize these effects. As a first step, we administered systemically anthrax lethal toxin (LeTx) and edema toxin (EdTx) to cohorts of three to twelve rats at different doses and determined the time of onset, degree of hypotension and mortality. We measured serum concentrations of the protective antigen (PA) toxin component at various time points after infusion. Peak serum levels of PA were in the µg/mL range with half-lives of 10–20 minutes. With doses that produced hypotension with delayed lethality, we then gave bolus intravenous infusions of toxins to groups of four to six instrumented rats and continuously monitored blood pressure by telemetry. Finally, the same doses used in the telemetry experiments were given to additional groups of four rats, and echocardiography was performed pretreatment and one, two, three and twenty-four hours post-treatment. LeTx and EdTx each produced hypotension. We observed a doubling of the velocity of propagation and 20% increases in left ventricular diastolic and systolic areas in LeTx-treated rats, but not in EdTx-treated rats. EdTx-but not LeTx-treated rats showed a significant increase in heart rate. These results indicate that LeTx reduced left ventricular systolic function and EdTx reduced preload. Uptake of toxins occurs readily into tissues with biological effects occurring within minutes to hours of serum toxin concentrations in the µg/mL range. LeTx and EdTx yield an irreversible shock with subsequent death. These findings should provide a basis for the rational design of drug interventions to reduce the dismal prognosis of systemic anthrax infections

Role of N-Terminal Amino Acids in the Potency of Anthrax Lethal Factor

Anthrax lethal factor (LF) is a Zn+2-dependent metalloprotease that cleaves several MAPK kinases and is responsible for the lethality of anthrax lethal toxin (LT). We observed that a recombinant LF (LF-HMA) which differs from wild type LF (LF-A) by the addition of two residues (His-Met) to the native Ala (A) terminus as a result of cloning manipulations has 3-fold lower potency toward cultured cells and experimental animals. We hypothesized that the “N-end rule”, which relates the half-life of proteins in cells to the identity of their N-terminal residue, might be operative in the case of LF, so that the N-terminal residue of LF would determine the cytosolic stability and thereby the potency of LF. Mutational studies that replaced the native N-terminal residue of LF with known N-end rule stabilizing or destabilizing residues confirmed that the N-terminal residue plays a significant role in determining the potency of LT for cultured cells and experimental animals. The fact that a commercially-available LF preparation (LF-HMA) that is widely used in basic research studies and for evaluation of vaccines and therapeutics is 3-fold less potent than native LF (LF-A) should be considered when comparing published studies and in the design of future experiments