Magnetoreception System in Honeybees (Apis mellifera)

Honeybees (Apis mellifera) undergo iron biomineralization, providing the basis for magnetoreception. We showed earlier the presence of superparamagnetic magnetite in iron granules formed in honeybees, and subscribed to the notion that external magnetic fields may cause expansion or contraction of the superparamagnetic particles in an orientation-specific manner, relaying the signal via cytoskeleton (Hsu and Li 1994). In this study, we established a size-density purification procedure, with which quantitative amount of iron granules was obtained from honey bee trophocytes and characterized; the density of iron granules was determined to be 1.25 g/cm(3). While we confirmed the presence of superparamagnetic magnetite in the iron granules, we observed changes in the size of the magnetic granules in the trophycytes upon applying additional magnetic field to the cells. A concomitant release of calcium ion was observed by confocal microscope. This size fluctuation triggered the increase of intracellular Ca(+2) , which was inhibited by colchicines and latrunculin B, known to be blockers for microtubule and microfilament syntheses, respectively. The associated cytoskeleton may thus relay the magnetosignal, initiating a neural response. A model for the mechanism of magnetoreception in honeybees is proposed, which may be applicable to most, if not all, magnetotactic organisms

Whole-cell-analysis of live cardiomyocytes using wide-field interferometric phase microscopy

We apply wide-field interferometric microscopy techniques to acquire quantitative phase profiles of ventricular cardiomyocytes in vitro during their rapid contraction with high temporal and spatial resolution. The whole-cell phase profiles are analyzed to yield valuable quantitative parameters characterizing the cell dynamics, without the need to decouple thickness from refractive index differences. Our experimental results verify that these new parameters can be used with wide field interferometric microscopy to discriminate the modulation of cardiomyocyte contraction dynamics due to temperature variation. To demonstrate the necessity of the proposed numerical analysis for cardiomyocytes, we present confocal dual-fluorescence-channel microscopy results which show that the rapid motion of the cell organelles during contraction preclude assuming a homogenous refractive index over the entire cell contents, or using multiple-exposure or scanning microscopy

The growth index of matter perturbations and modified gravity

We place tight constraints on the growth index $\gamma$ by using the recent growth history results of 2dFGRS, SDSS-LRG, VIMOS-VLT deep Survey (VVDS) and {\em WiggleZ} datasets. In particular, we investigate several parametrizations of the growth index $\gamma(z)$, by comparing their cosmological evolution using observational growth rate data at different redshifts. Utilizing a standard likelihood analysis we find that the use of the combined growth data provided by the 2dFGRS, SDSS-LRG, VVDS and {\em WiggleZ} galaxy surveys, puts the most stringent constraints on the value of the growth index. As an example, assuming a constant growth index we obtain that $\gamma=0.602\pm 0.055$ for the concordance $\Lambda$CDM expansion model. Concerning the Dvali-Gabadadze-Porrati gravity model, we find $\gamma=0.503\pm 0.06$ which is lower, and almost $3\sigma$ away, from the theoretically predicted value of $\gamma_{DGP}\simeq 11/16$. Finally, based on a time varying growth index we also confirm that the combined growth data disfavor the DGP gravity.Comment: 8 pages, 5 figures. Revised version accepted in MNRAS. arXiv admin note: text overlap with arXiv:1202.163

CPTCPT Violating Electrodynamics and Chern-Simons Modified Gravity

The electrodynamics with a Chern-Simons term $p_{\mu}A_{\nu}\widetilde{F}^{\mu\nu}$ violates Lorentz and $CPT$ symmetries with a non-vanishing $p_{\mu}$. For a fixed vector $p_{\mu}$, in this paper we point out that the energy-momentum tensor of this theory coupled to the gravity minimally is symmetric but not divergence free, which consequently makes the gravitational field equation inconsistent. To preserve the consistency, we introduce a Chern-Simons term in the gravity sector with the coefficient determined by the Lorentz and $CPT$ violating term in the electromagnetic field. Further we study the phenomenologies of the model on the cosmic microwave background radiation and the relic gravitational waves.Comment: 11 pages, 1 figure, the version to appear in Physics Letters

Long-Term Storage Effects on Stability of Aβ1–40, Aβ1–42, and Total Tau Proteins in Human Plasma Samples Measured with Immunomagnetic Reduction Assays

Background: The stability of Alzheimer’s disease (AD) biomarkers in plasma, measured by immunomagnetic reduction (IMR) after long-term storage at –80°C, has not been established before. Method: Ninety-nine human plasma samples from 53 normal controls (NCs), 5 patients with amnestic mild cognitive impairment (aMCI), and 41 AD patients were collected. Each plasma sample was aliquoted and stored as single-use aliquots at –80°C. The baseline measurements for Aβ1–40, Aβ1–42, and total Tau protein (T-Tau) concentrations for each sample were done within 3 months of blood draw by IMR. They are referred to as baseline concentrations. A separate aliquot from each sample was assayed with IMR to assess the stability of the measured analytes during storage at –80°C between 1.1 and 5.4 years. This is referred to as a repeated result. Results: IMR shows that plasma levels of Aβ1–40 and Aβ1–42 exhibit stability over 5-year storage at –80°C and that plasma levels of T-Tau are less stable (approximately 1.5 years). Conclusion: Although the measured concentrations of T-Tau in human plasma may alter during storage, the diagnostic utility of the results are only slightly affected when the product of Aβ1–42 and T-Tau concentrations are used. The results show that the overall agreement between baseline and repeated measurements in the ability of discriminating NCs from aMCI/AD patients is higher than 80%

Direct involvement of the TEN domain at the active site of human telomerase

Telomerase is a ribonucleoprotein that adds DNA to the ends of chromosomes. The catalytic protein subunit of telomerase (TERT) contains an N-terminal domain (TEN) that is important for activity and processivity. Here we describe a mutation in the TEN domain of human TERT that results in a greatly increased primer Kd, supporting a role for the TEN domain in DNA affinity. Measurement of enzyme kinetic parameters has revealed that this mutant enzyme is also defective in dNTP polymerization, particularly while copying position 51 of the RNA template. The catalytic defect is independent of the presence of binding interactions at the 5′-region of the DNA primer, and is not a defect in translocation rate. These data suggest that the TEN domain is involved in conformational changes required to position the 3′-end of the primer in the active site during nucleotide addition, a function which is distinct from the role of the TEN domain in providing DNA binding affinity

Immobilization of enzyme and antibody on ALD-HfO2-EIS structure by NH3 plasma treatment

Thin hafnium oxide layers deposited by an atomic layer deposition system were investigated as the sensing membrane of the electrolyte-insulator-semiconductor structure. Moreover, a post-remote NH3 plasma treatment was proposed to replace the complicated silanization procedure for enzyme immobilization. Compared to conventional methods using chemical procedures, remote NH3 plasma treatment reduces the processing steps and time. The results exhibited that urea and antigen can be successfully detected, which indicated that the immobilization process is correct

The growth of linear perturbations in the DGP model

We study the linear growth of matter perturbations in the DGP model with the growth index $\gamma$ as a function of redshift. At the linear approximation: $\gamma(z)\approx\gamma_0+\gamma_0^\prime z$, we find that, for $0.2\leq\Omega_{m,0}\leq0.35$, $\gamma_0$ takes the value from 0.658 to 0.671, and $\gamma_0^\prime$ ranges from 0.035 to 0.042. With three low redshift observational data of the growth factor, we obtain the observational constraints on $\gamma_0$ and $\gamma_0'$ for the $\Lambda CDM$ and DGP models and find that the observations favor the $\Lambda CDM$ model but at the $1\sigma$ confidence level both the $\Lambda CDM$ and DGP models are consistent with the observations.Comment: 12 pages, 4 figuers, to appear in PL

The growth factor of matter perturbations in an f(R) gravity

The growth of matter perturbations in the $f(R)$ model proposed by Starobinsky is studied in this paper. Three different parametric forms of the growth index are considered respectively and constraints on the model are obtained at both the $1\sigma$ and $2\sigma$ confidence levels, by using the current observational data for the growth factor. It is found, for all the three parametric forms of the growth index examined, that the Starobinsky model is consistent with the observations only at the $2\sigma$ confidence level.Comment: 15 pages, 5 figure

CDK5 Is Essential for Soluble Amyloid β-Induced Degradation of GKAP and Remodeling of the Synaptic Actin Cytoskeleton

The early stages of Alzheimer's disease are marked by synaptic dysfunction and loss. This process results from the disassembly and degradation of synaptic components, in particular of scaffolding proteins that compose the post-synaptic density (PSD), namely PSD95, Homer and Shank. Here we investigated in rat frontal cortex dissociated culture the mechanisms involved in the downregulation of GKAP (SAPAP1), which links the PSD95 complex to the Shank complex and cytoskeletal structures within the PSD. We show that Aβ causes the rapid loss of GKAP from synapses through a pathway that critically requires cdk5 activity, and is set in motion by NMDAR activity and Ca2+ influx. We show that GKAP is a direct substrate of cdk5 and that its phosphorylation results in polyubiquitination and proteasomal degradation of GKAP and remodeling (collapse) of the synaptic actin cytoskeleton; the latter effect is abolished in neurons expressing GKAP mutants that are resistant to phosphorylation by cdk5. Given that cdk5 also regulates degradation of PSD95, these results underscore the central position of cdk5 in mediating Aβ-induced PSD disassembly and synapse loss