Back-action Induced Non-equilibrium Effect in Electron Charge Counting Statistics

We report our study of the real-time charge counting statistics measured by a quantum point contact (QPC) coupled to a single quantum dot (QD) under different back-action strength. By tuning the QD-QPC coupling or QPC bias, we controlled the QPC back-action which drives the QD electrons out of thermal equilibrium. The random telegraph signal (RTS) statistics showed strong and tunable non-thermal-equilibrium saturation effect, which can be quantitatively characterized as a back-action induced tunneling out rate. We found that the QD-QPC coupling and QPC bias voltage played different roles on the back-action strength and cut-off energy.Comment: 4 pages, 4 figures, 1 tabl

Population analysis of CD4+ T cell chemokine receptor transcript expression during in vivo typeâ 1 (mycobacterial) and typeâ 2 (schistosomal) immune responses

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141990/1/jlb0363.pd

Neuron-Specific HuR-Deficient Mice Spontaneously Develop Motor Neuron Disease

Human Ag R (HuR) is an RNA binding protein in the ELAVL protein family. To study the neuron-specific function of HuR, we generated inducible, neuron-specific HuR-deficient mice of both sexes. After tamoxifen-induced deletion of HuR, these mice developed a phenotype consisting of poor balance, decreased movement, and decreased strength. They performed significantly worse on the rotarod test compared with littermate control mice, indicating coordination deficiency. Using the grip-strength test, it was also determined that the forelimbs of neuron-specific HuR-deficient mice were much weaker than littermate control mice. Immunostaining of the brain and cervical spinal cord showed that HuR-deficient neurons had increased levels of cleaved caspase-3, a hallmark of cell apoptosis. Caspase-3 cleavage was especially strong in pyramidal neurons and α motor neurons of HuR-deficient mice. Genome-wide microarray and real-time PCR analysis further indicated that HuR deficiency in neurons resulted in altered expression of genes in the brain involved in cell growth, including trichoplein keratin filament-binding protein, Cdkn2c, G-protein signaling modulator 2, immediate early response 2, superoxide dismutase 1, and Bcl2. The additional enriched Gene Ontology terms in the brain tissues of neuron-specific HuR-deficient mice were largely related to inflammation, including IFN-induced genes and complement components. Importantly, some of these HuR-regulated genes were also significantly altered in the brain and spinal cord of patients with amyotrophic lateral sclerosis. Additionally, neuronal HuR deficiency resulted in the redistribution of TDP43 to cytosolic granules, which has been linked to motor neuron disease. Taken together, we propose that this neuron-specific HuR-deficient mouse strain can potentially be used as a motor neuron disease model

The Photometric System of Tsinghua-NAOC 80-cm Telescope at NAOC Xinglong Observatory

Tsinghua-NAOC (National Astronomical Observatories of China) Telescope (hereafter, TNT) is an 80-cm Cassegrain reflecting telescope located at Xinglong bservatory of NAOC, with main scientific goals of monitoring various transients in the universe such as supernovae, gamma-ray bursts, novae, variable stars, and active galactic nuclei. We present in this paper a systematic test and analysis of the photometric performance of this telescope. Based on the calibration observations on twelve photometric nights, spanning the period from year 2004 to year 2012, we derived an accurate transformation relationship between the instrumental $ubvri$ magnitudes and standard Johnson $UBV$ and Cousins $RI$ magnitudes. In particular, the color terms and the extinction coefficients of different passbands are well determined. With these data, we also obtained the limiting magnitudes and the photometric precision of TNT. It is worthwhile to point out that the sky background at Xinglong Observatory may become gradually worse over the period from year 2005 to year 2012 (e.g., $\sim$21.4 mag vs. $\sim$20.1 mag in the V band).Comment: 12 pages,9 figures, accepted by RA

Direct CP violation of B→lνB \to l \nu in unparticle physics

We have investigated the effects of unparticles in decays $B \to l \nu$. It is found that the direct CP violation in the decays, which is zero in SM, can show up due to the CP conserving phase intrinsic in unparticle physics. For $l=\tau$, the direct CP asymmetry can reach 30% for the scalar unparticle contribution, and 100% for the longitudinal vector unparticle contribution under the constraints of ${\rm Br}(B\to\tau\nu)$ and $\nu e$ elastic scattering. If both unparticle-lepton coupling universality and unparticle-quark coupling universality are assumed the constraint from $Br(\pi\to \mu\nu)$ leads that the direct CP violation in $B\to l\nu$ can only reach at most 8% and 1% for scalar and vector unparticle contributions respectively if $d_{\cal U} < 2$. If the direct CP violation is observed in the future it would give strong evidence for the existence of unparticle stuff.Comment: 9 pages, 2 figures, to appear in PR

Close Functional Coupling Between Ca(2+) Release-Activated Ca(2+) Channels and Reactive Oxygen Species Production in Murine Macrophages

Aim. To investigate the role of Ca(2+) release-activated Ca(2+) (CRAC) channels in the ROS production in macrophages. Methods. The intracellular [Ca(2+)](i) was analyzed by confocal laser microscopy. The production of ROS was assayed by flow cytometry. Results. Both LPS and thapsigargin induced an increase in intracellular [Ca(2+)](i), either in the presence or absence of extracellular Ca(2+) in murine macrophages. The Ca(2+) signal was sustained in the presence of external Ca(2+) and only initiated a mild and transient rise in the absence of external Ca(2+). CRAC channel inhibitor 2-APB completely suppressed the Ca(2+) entry signal evoked by thapsigargin, and suppressed approximately 93% of the Ca(2+) entry signal evoked by LPS. The increase in intracellular [Ca(2+)](i) was associated with increased ROS production, which was completely abolished in the absence of extracellular Ca(2+) or in the presence of CRAC channel inhibitors 2-APB and Gd(3+). The mitochondrial uncoupler carbonyl cyanide p-trifluoromethoxy-phenylhydrazone and the inhibitor of the electron transport chain, antimycin, evoked a marked increase in ROS production and completely inhibited thapsigargin and LPS-evoked responses. Conclusions. These findings indicate that the LPS-induced intracellular [Ca(2+)](i) increase depends on the Ca(2+) entry through CRAC channels, and close functional coupling between CRAC and ROS production in murine macrophages

DNA-PKcs plays a dominant role in the regulation of H2AX phosphorylation in response to DNA damage and cell cycle progression

<p>Abstract</p> <p>Background</p> <p>When DNA double-strand breaks (DSB) are induced by ionizing radiation (IR) in cells, histone H2AX is quickly phosphorylated into γ-H2AX (p-S139) around the DSB site. The necessity of DNA-PKcs in regulating the phosphorylation of H2AX in response to DNA damage and cell cycle progression was investigated.</p> <p>Results</p> <p>The level of γH2AX in HeLa cells increased rapidly with a peak level at 0.25 - 1.0 h after 4 Gy γ irradiation. SiRNA-mediated depression of DNA-PKcs resulted in a strikingly decreased level of γH2AX. An increased γH2AX was also induced in the ATM deficient cell line AT5BIVA at 0.5 - 1.0 h after 4 Gy γ rays, and this IR-increased γH2AX in ATM deficient cells was dramatically abolished by the PIKK inhibitor wortmannin and the DNA-PKcs specific inhibitor NU7026. A high level of constitutive expression of γH2AX was observed in another ATM deficient cell line ATS4. The alteration of γH2AX level associated with cell cycle progression was also observed. HeLa cells with siRNA-depressed DNA-PKcs (HeLa-H1) or normal level DNA-PKcs (HeLa-NC) were synchronized at the G1 phase with the thymidine double-blocking method. At ~5 h after the synchronized cells were released from the G1 block, the S phase cells were dominant (80%) for both HeLa-H1 and HeLa-NC cells. At 8 - 9 h after the synchronized cells released from the G1 block, the proportion of G2/M population reached 56 - 60% for HeLa-NC cells, which was higher than that for HeLa H1 cells (33 - 40%). Consistently, the proportion of S phase for HeLa-NC cells decreased to ~15%; while a higher level (26 - 33%) was still maintained for the DNA-PKcs depleted HeLa-H1 cells during this period. In HeLa-NC cells, the γH2AX level increased gradually as the cells were released from the G1 block and entered the G2/M phase. However, this γH2AX alteration associated with cell cycle progressing was remarkably suppressed in the DNA-PKcs depleted HeLa-H1 cells, while wortmannin and NU7026 could also suppress this cell cycle related phosphorylation of H2AX. Furthermore, inhibition of GSK3β activity with LiCl or specific siRNA could up-regulate the γH2AX level and prolong the time of increased γH2AX to 10 h or more after 4 Gy. GSK3β is a negative regulation target of DNA-PKcs/Akt signaling via phosphorylation on Ser9, which leads to its inactivation. Depression of DNA-PKcs in HeLa cells leads to a decreased phosphorylation of Akt on Ser473 and its target GSK3β on Ser9, which, in other words, results in an increased activation of GSK3β. In addition, inhibition of PDK (another up-stream regulator of Akt/GSK3β) by siRNA can also decrease the induction of γH2AX in response to both DNA damage and cell cycle progression.</p> <p>Conclusion</p> <p>DNA-PKcs plays a dominant role in regulating the phosphorylation of H2AX in response to both DNA damage and cell cycle progression. It can directly phosphorylate H2AX independent of ATM and indirectly modulate the phosphorylation level of γH2AX via the Akt/GSK3 β signal pathway.</p