Elimination of degenerate trajectory of single atom strongly coupled to the tilted cavity TEM10 mode

We demonstrate the trajectory measurement of the single neutral atoms deterministically using a high-finesse optical micro-cavity. Single atom strongly couples to the high-order transverse vacuum TEM_{10} mode, instead of the usual TEM_{00} mode, and the parameter of the system is (g_{10},\kappa ,\gamma )=2\pi \times (20.5,2.6,2.6)MHz. The atoms simply fall down freely from the magneto-optic trap into the cavity modes and the trajectories of the single atoms are linear. The transmission spectrums of atoms passing through the TEM10 mode are detected by a single photon counting modules and well fitted. Thanks to the tilted cavity transverse TEM10 mode, which is inclined to the vertical direction about 45 degrees and it helps us, for the first time, to eliminate the degenerate trajectory of the single atom falling through the cavity and get the unique atom trajectory. Atom position with high precision of 0.1{\mu}m in the off-axis direction (axis y) is obtained, and the spatial resolution of 5.6{\mu}m is achieved in time of 10{\mu}s along the vertical direction (axis x). The average velocity of the atoms is also measured from the atom transits, which determines the temperature of the atoms in magneto-optic trap, 186{\mu}K {\pm} 19{\mu}K.Comment: 13 pages, 5figure

Hypoglycemia and Death in Mice Following Experimental Exposure to an Extract of Trogia venenata Mushrooms

BACKGROUND: Clusters of sudden unexplained death (SUD) in Yunnan Province, China, have been linked to eating Trogia venenata mushrooms. We evaluated the toxic effect of this mushroom on mice. METHODS: We prepared extracts of fresh T. venenata and Laccaria vinaceoavellanea mushrooms collected from the environs of a village that had SUD. We randomly allocated mice into treatment groups and administered mushroom extracts at doses ranging from 500 to 3500 mg/kg and water (control) via a gavage needle. We observed mice for mortality for 7 days after a 3500 mg/kg dose and for 24 hours after doses from 500 to 3000 mg/kg. We determined biochemical markers from serum two hours after a 2000 mg/kg dose. RESULTS: Ten mice fed T. venenata extract (3500 mg/kg) died by five hours whereas all control mice (L. vinaceoavellanea extract and water) survived the seven-day observation period. All mice died by five hours after exposure to single doses of T. venenata extract ranging from 1500 to 3000 mg/kg, while the four mice exposed to a 500 mg/kg dose all survived. Mice fed 2000 mg/kg of T. venenata extract developed profound hypoglycemia (median= 0.66 mmol/L) two hours after exposure. DISCUSSION: Hypoglycemia and death within hours of exposure, a pattern unique among mushroom toxicity, characterize T. venenata poisoning

Lack of Association of miR-146a rs2910164 Polymorphism with Gastrointestinal Cancers: Evidence from 10206 Subjects

BACKGROUND: Recent studies on the association between miR-146a rs2910164 polymorphism and risk of gastrointestinal (GI) cancers showed inconclusive results. Accordingly, we conducted a comprehensive literature search and a meta-analysis to clarify the association. METHODOLOGY/PRINCIPAL FINDINGS: Data were collected from the following electronic databases: Pubmed, Excerpta Medica Database (Embase), and Chinese Biomedical Literature Database (CBM), with the last report up to February 24, 2012. The odds ratio (OR) and its 95% confidence interval (95%CI) were used to assess the strength of association. Ultimately, a total of 12 studies (4,817 cases and 5,389 controls) were found to be eligible for meta-analysis. We summarized the data on the association between miR-146a rs2910164 polymorphism and risk of GI cancers in the overall population, and performed subgroup analyses by ethnicity, cancer types, and quality of studies. In the overall analysis, there was no evidence of association between miR-146a rs2910164 polymorphism and the risk of GI cancers (G versus C: OR = 1.07, 95%CI 0.98-1.16, P = 0.14; GG+GC versus CC: OR = 1.14, 95%CI 1.00-1.31, P = 0.05; GG versus GC+CC: OR = 1.06, 95%CI 0.91-1.23, P = 0.47; GG versus CC: OR = 1.17, 95%CI 0.95-1.44, P = 0.13; GC versus CC: OR = 1.14, 95%CI 1.00-1.31, P = 0.05). Similar results were found in the subgroup analyses by ethnicity, cancer types, and quality of studies. CONCLUSIONS/SIGNIFICANCE: This meta-analysis demonstrates that miR-146a rs2910164 polymorphism is not associated with GI cancers susceptibility. More well-designed studies based on larger sample sizes and homogeneous cancer patients are needed

A Novel Function of Apolipoprotein E: Upregulation of ATP-Binding Cassette Transporter A1 Expression

Despite the well known importance of apolipoprotein (Apo) E in cholesterol efflux, the effect of ApoE on the expression of ATP-binding cassette transporter A1 (ABCA1) has never been investigated. The objective of this study was to determine the effect of ApoE on ApoB-carrying lipoprotein-induced expression of ABCA1, a protein that mediates cholesterol efflux. Our data demonstrate that ApoB-carrying lipoproteins obtained from both wild-type and ApoE knockout mice induced ApoAI-mediated cholesterol efflux in mouse macrophages, which was associated with an enhanced ABCA1 promoter activity, and an increased ABCA1 mRNA and protein expression. In addition, these lipoproteins increased the level of phosphorylated specificity protein 1 (Sp1) and the amount of Sp1 bound to the ABCA1 promoter. However, all these inductions were significantly diminished in cells treated with ApoE-free lipoproteins, when compared to those treated with wild-type lipoproteins. Enrichment with human ApoE3 reversed the reduced inducibility of ApoE-free lipoproteins. Moreover, we observed that inhibition of Sp1 DNA-binding by mithramycin A diminished ABCA1 expression and ApoAI-mediated cholesterol efflux induced by ApoB-carrying lipoproteins, and that mutation of the Sp1-binding motif in the ABCA1 promoter region diminished ApoB-carrying lipoprotein-induced ABCA1 promoter activity. Collectively, these data suggest that ApoE associated with ApoB-carrying lipoproteins has an upregulatory role on ABCA1 expression, and that induction of Sp1 phosphorylation is a mechanism by which ApoE upregulates ABCA1 expression

TRAF6 Promotes Myogenic Differentiation via the TAK1/p38 Mitogen-Activated Protein Kinase and Akt Pathways

p38 mitogen-activated protein kinase (MAPK) is an essential kinase involved in myogenic differentiation. Although many substrates of p38 MAPK have been identified, little is known about its upstream activators during myogenic differentiation. TRAF6 is known to function in cytokine signaling during inflammatory responses. However, not much is known about its role in myogenic differentiation and muscle regeneration. We showed here that TRAF6 and its intrinsic ubiquitin E3 ligase activity are required for myogenic differentiation. In mouse myoblasts, knockdown of TRAF6 compromised the p38 MAPK and Akt pathways, while deliberate activation of either pathway rescued the differentiation defect caused by TRAF6 knockdown. TAK1 acted as a key signal transducer downstream of TRAF6 in myogenic differentiation. In vivo, knockdown of TRAF6 in mouse muscles compromised the injury-induced muscle regeneration without impairing macrophage infiltration and myoblast proliferation. Collectively, we demonstrated that TRAF6 promotes myogenic differentiation and muscle regeneration via the TAK1/p38 MAPK and Akt pathways