Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
332,270
result(s) for
"X"
Sort by:
Ultrahigh-energy photons up to 1.4 petaelectronvolts from 12 γ-ray Galactic sources
The extension of the cosmic-ray spectrum beyond 1 petaelectronvolt (PeV; 10
15
electronvolts) indicates the existence of the so-called PeVatrons—cosmic-ray factories that accelerate particles to PeV energies. We need to locate and identify such objects to find the origin of Galactic cosmic rays
1
. The principal signature of both electron and proton PeVatrons is ultrahigh-energy (exceeding 100 TeV) γ radiation. Evidence of the presence of a proton PeVatron has been found in the Galactic Centre, according to the detection of a hard-spectrum radiation extending to 0.04 PeV (ref.
2
). Although γ-rays with energies slightly higher than 0.1 PeV have been reported from a few objects in the Galactic plane
3
–
6
, unbiased identification and in-depth exploration of PeVatrons requires detection of γ-rays with energies well above 0.1 PeV. Here we report the detection of more than 530 photons at energies above 100 teraelectronvolts and up to 1.4 PeV from 12 ultrahigh-energy γ-ray sources with a statistical significance greater than seven standard deviations. Despite having several potential counterparts in their proximity, including pulsar wind nebulae, supernova remnants and star-forming regions, the PeVatrons responsible for the ultrahigh-energy γ-rays have not yet been firmly localized and identified (except for the Crab Nebula), leaving open the origin of these extreme accelerators.
Observations of γ-rays with energies up to 1.4 PeV find that 12 sources in the Galaxy are PeVatrons, one of which is the Crab Nebula.
Journal Article
Realization of a crosstalk-avoided quantum network node using dual-type qubits of the same ion species
Generating ion-photon entanglement is a crucial step for scalable trapped-ion quantum networks. To avoid the crosstalk on memory qubits carrying quantum information, it is common to use a different ion species for ion-photon entanglement generation such that the scattered photons are far off-resonant for the memory qubits. However, such a dual-species scheme can be subject to inefficient sympathetic cooling due to the mass mismatch of the ions. Here we demonstrate a trapped-ion quantum network node in the dual-type qubit scheme where two types of qubits are encoded in the
S
and
F
hyperfine structure levels of
171
Yb
+
ions. We generate ion photon entanglement for the
S
-qubit in a typical timescale of hundreds of milliseconds, and verify its small crosstalk on a nearby
F
-qubit with coherence time above seconds. Our work demonstrates an enabling function of the dual-type qubit scheme for scalable quantum networks.
In ion-photon quantum network platforms, usually memory qubits and communication qubits are encoded in ions of different species. Here, instead, the authors show how to realise ion-photon entanglement within the same-species-dual-encoding scheme.
Journal Article
α4 is highly expressed in carcinogen-transformed human cells and primary human cancers
A regulator of the protein phosphatase 2A (PP2A), α4, has been implicated in a variety of functions that regulate many cellular processes. To explore the role of α4 in human cell transformation and tumorigenesis, we show that α4 is highly expressed in human cells transformed by chemical carcinogens including benzo(
a
)pyrene, aflatoxin B
1
,
N
-methyl-
N
′-nitro-
N
-nitrosoguanidine, nickel sulfate and in several hepatic and lung cancer cell lines. In addition, overexpression of α4 was detected in 87.5% (74/80) of primary hepatocellular carcinomas, 84.0% (21/25) of primary lung cancers and 81.8% (9/11) of primary breast cancers, indicating that α4 is ubiquitously highly expressed in human cancer. Functional studies revealed that elevated α4 expression results in an increase in cell proliferation, promotion of cell survival and decreased PP2A-attributable activity. Importantly, ectopic expression of α4 permits non-transformed human embryonic kidney cells (HEKTER) and L02R cells to form tumors in immunodeficient mice. Furthermore, we show that the highly expressed α4 in transformed cells or human tumors is not regulated by DNA hypomethylation. A microRNA, miR-34b, that suppresses the expression of α4 through specific binding to the 3′-untranslated region of α4 is downregulated in transformed or human lung tumors. Taken together, these observations identify that α4 possesses an oncogenic function. Reduction of PP2A activity due to an enhanced α4–PP2A interaction contributes directly to chemical carcinogen-induced tumorigenesis.
Journal Article
The last summer of the Death Warriors
Seventeen-year-old Pancho is bent on avenging the senseless death of his sister, but after he meets D.Q, who is dying of cancer, and Marisol, one of D.Q.'s caregivers, both boys find their lives changed by their interactions.
Book
Observation of a robust zero-energy bound state in iron-based superconductor Fe(Te,Se)
The symmetry of Cooper pairs in iron-based superconductors is an issue under continued investigation. A scanning tunnelling study of Fe(Te,Se) reveals a robust zero-energy bound state, providing evidence for a non-trivial pairing symmetry.
In superconductors, electrons are paired and condensed into the ground state. An impurity can break the electron pairs into quasiparticles with energy states inside the superconducting gap. The characteristics of such in-gap states reflect accordingly the properties of the superconducting ground state
1
. A zero-energy in-gap state is particularly noteworthy, because it can be the consequence of non-trivial pairing symmetry
1
or topology
2
,
3
. Here we use scanning tunnelling microscopy/spectroscopy to demonstrate that an isotropic zero-energy bound state with a decay length of ∼10 Å emerges at each interstitial iron impurity in superconducting Fe(Te,Se). More noticeably, this zero-energy bound state is robust against a magnetic field up to 8 T, as well as perturbations by neighbouring impurities. Such a spectroscopic feature has no natural explanation in terms of impurity states in superconductors with
s
-wave symmetry, but bears all the characteristics of the Majorana bound state proposed for topological superconductors
2
,
3
, indicating that the superconducting state and the scattering mechanism of the interstitial iron impurities in Fe(Te,Se) are highly unconventional.
Journal Article
Canto hondo = Deep song
\"This is a collection of 100 poems in both English and Spanish inspired by the Spanish poet Federico Garcâia Lorca\"--Provided by publisher.
Book
EBV-miR-BART7-3p promotes the EMT and metastasis of nasopharyngeal carcinoma cells by suppressing the tumor suppressor PTEN
The epithelial-mesenchymal transition (EMT) is crucial to cancer progression and metastasis. Although multiple cellular miRNAs have been identified to regulate the EMT and metastasis in cancers, the role of viral miRNAs in cancer progression remains largely unknown. Nasopharyngeal carcinoma (NPC) is an Epstein-Barr virus (EBV)-associated malignancy typically characterized by its early metastasis. In the present study, we have discovered the involvement of a viral miRNA, EBV-miR-BART7-3p, in the EMT and metastasis of NPC cells. Initially, we observed that EBV-miR-BART7-3p was highly expressed in NPC and positively correlated with lymph node metastasis and clinical stage of NPC. Subsequently, we demonstrated that EBV-miR-BART7-3p enhanced cell migration/invasion
in vitro
, cancer metastasis
in vivo
, and particularly the EMT characterized by loss of epithelial markers and gain of mesenchymal features in NPC cells. Furthermore, mechanistic studies disclosed that EBV-miR-BART7-3p targeted a major human tumor suppressor PTEN, modulating PI3K/Akt/GSK-3β signaling and eventually leading to the high expression and nuclear accumulation of Snail and β-catenin, which favor EMT. Knockdown of PTEN could phenocopy the effect of EBV-miR-BART7-3p, whereas re-expression of PTEN resulted in a phenotypic reversion. Moreover, these findings were supported by an observation of an EBV-positive cell model in which silencing of endogenous EBV-miR-BART7-3p partially attenuated cell migration/invasion and altered EMT protein expression pattern via reverting PI3K/Akt, Snail and β-catenin expression. Thus, this study suggests a novel mechanism by which EBV-miR-BART7-3p modulates the EMT and metastasis of NPC cells, and a clinical implication of EBV-miR-BART7-3p as a potential biomarker or therapeutic target.
Journal Article