5,736 research outputs found
Spin entanglement induced by spin-orbit interactions in coupled quantum dots
We theoretically explore the possibility of creating spin quantum
entanglement in a system of two electrons confined respectively in two
vertically coupled quantum dots in the presence of Rashba type spin-orbit
coupling. We find that the system can be described by a generalized Jaynes -
Cummings model of two modes bosons interacting with two spins. The lower
excitation states of this model are calculated to reveal the underlying physics
of the far infrared absorption spectra. The analytic perturbation approach
shows that an effective transverse coupling of spins can be obtained by
eliminating the orbital degrees of freedom in the large detuning limit. Here,
the orbital degrees of freedom of the two electrons, which are described by two
modes of bosons, serve as a quantized data bus to exchange the quantum
information between two electrons. Then a nontrivial two-qubit logic gate is
realized and spin entanglement between the two electrons is created by virtue
of spin-orbit coupling.Comment: 7 pages, 5 figure
Białko CTRP3 zwiększa wrażliwość na insulinę adipocytów 3T3-L1 przez hamowanie procesu zapalnego i poprawę przekazywania sygnału insulinowego
Introduction: C1q/TNF-related Protein-3 (CTRP3) is a novel adipokine with multiple effects such as lowering glucose levels, inhibiting glyconeogenesis in the liver, and increasing angiogenesis and anti-inflammation. But little is known about the effects of CTRP3 on insulin resistance in adipose tissue. This study aims to investigate the effects and mechanisms of CTRP3 on the insulin sensitivity of 3T3-L1 adipocytes.Material and methods: Insulin resistant 3T3-L1 adipocytes were induced by palmic acid cultivation. Such adipocytes were treated with recombinant CTRP3 protein at different concentrations (0, 10, 50, 1,250 ng/mL)for 12 hours, and at a concentration of 250 ng/mL for differing times (2, 6, 12, and 24h). Another group was pre-treated with wortmannin, the special inhibitor of phosphatidylinositol-4,5- bisphosphate 3-kinase (PI3K), for 20 minutes before the treatment with 250 ng/mL CTRP3. The glucose consumption, the glucose uptake, the expression and release of tumour necrosis factor α (TNF-α) and interleukin-6(IL-6) in supernatant, and the protein relative expression of PI3K and protein kinase B (PKB)(ser437) were detected.Results: Compared to the control group, glucose consumption in the CTRP3 intervention group at concentrations of 10, 50, 250, and 1,250 ng/mL was increased by 22.1%, 42.9%, 76.6% and 80.5% respectively (all P < 0.01); the glucose uptake was increased by 39.0%, 68.0%, 108.0% and 111.0% respectively (all P < 0.01); the content of TNF-α in the culture media of CTRP3 (10, 50, 250 ng/mL) intervention group was decreased by 7.6% (P > 0.05), 13.0% (P < 0.05) and 17.4% (P < 0.01) respectively; the content of IL-6 was decreased by 7.1%, 12.4% and 17.1% respectively (all P < 0.01); the protein relative expression of PI3K was increased by 0.63-, 1.00- and 1.36-fold respectively (all P < 0.01), and PKB(ser437) increased by 0.65-, 1.61- and 1.93-fold respectively (all P < 0.01); the mRNA relative expression of GLUT-4 was increased by 23.0%, 47.0% and 62.0% respectively (all P < 0.01). After the treatment with wortmannin, glucose consumption, glucose uptake, PI3K and PKB(ser437) protein relative expression, as well as GLUT-4 mRNA relative expression, was decreased by 53.2%, 44.7%, 43.4%, 56.1 and 30.9% respectively (all P < 0.01).Conclusions: CTRP3 could improve insulin sensitivity of insulin resistant 3T3-L1 adipocytes by decreasing inflammation and ameliorating insulin signalling transduction, indicating that CTRP3 may be a new target for the prevention and cure of insulin resistance and type 2 diabetes. (Endokrynol Pol 2014; 65 (4): 252–258) Wstęp: Białko związane z C1q/TNF typu 3 (CTRP3, C1q/TNF-related Protein-3) jest nowo odkrytą adipokiną o wielorakim działaniu obejmującym obniżenie stężenia glukozy we krwi, hamowanie glukoneogenezy w wątrobie, pobudzanie angiogenezy i działanie przeciwzapalne, Niewiele jednak wiadomo na temat wpływu CTRP3 na insulinooporność komórek tłuszczowych. Badanie to przeprowadzono w celu oceny mechanizmów działania tej adipokiny i jej wpływu na wrażliwość na insulinę adipocytów 3T3-L1.Materiał i metody: Insulinooporne adipocyty 3T3-L1 uzyskano poprzez dodanie do hodowli tych komórek kwasu palmitynowego. Następnie adipocyty te poddano działaniu rekombinowanego białka CTRP3 w różnych stężeniach (0, 10, 50, 1250 ng/ml przez 12 godzin oraz w stężeniu 250 ng/ml przez różny czas (2, 6, 12, 24 godz.). Inną grupę hodowli komórkowych przed dodaniem CTRP3 w stężeniu 250 ng/ml inkubowano wstępnie z wortmaniną, inhibitorem kinazy fosfatydyloinozytolu-4,5 (PI3K, phosphatidylinositol-4,5- bisphosphate 3-kinase) przez 20 minut. Określono zużycie glukozy, wychwyt glukozy, ekspresję i uwalnianie czynnika martwicy nowotworów typu alfa (TNF-α, tumor necrosis factor α) i interleukiny 6 (IL-6, interleukin-6,) w supernatancie oraz ekspresję PI3K i kinazy białkowej B (PKB, protein kinase B) (ser437).Wyniki: Zużycie glukozy w hodowlach poddanych działaniu CTRP3 w stężeniach 10, 50, 250, 1250 ng/ml było większe niż w hodowli kontrolnej odpowiednio o 22,1%, 42,9%, 76,6% i 80,5% (dla wszystkich porównań p < 0,01). Wychwyt glukozy był większy o 39,0%, 68,0%, 108,0% i 111,0% (dla wszystkich porównań p < 0,01) Zawartości TNF-α w medium hodowli komórkowej z dodatkiem CTRP3 (10, 50, 250 ng/ml) były mniejsze odpowiednio o 7,6% (p > 0,05), 13,0% (p < 0,05) i 17,4% (p < 0,01), a zawartości IL-6 były mniejsze o odpowiednio 7,1%, 12,4% i 17,1% (dla wszystkich porównań p < 0,01). Związana z białkami ekspresja PI3K stanowiła odpowiednio 0,63-, 1,00- i 1,36-krotność wartości uzyskanej w hodowli kontrolnej (dla wszystkich porównań p < 0,01), a ekspresja PKB(ser437) stanowiła odpowiednio 0,65-, 1,61- i 1,93-krotność (dla wszystkich porównań p < 0,01); Względna ekspresja mRNA GLUT-4 była większa odpowiednio o 23,0%, 47,0% i 62,0% (dla wszystkich porównań p < 0,01). W hodowlach poddanych wstępnie działaniu wortmaniny zużycie glukozy, signifiwychwyt glukozy, ekspresja PI3K i PKB(ser437) oraz ekspresja mRNA GLUT-4 były mniejsze odpowiednio o 53,2%, 44,7%, 43,4%, 56,1% i 30,9% (dla wszystkich porównań p < 0,01).Wnioski: Białko CTRP3 może powodować zwiększenie wrażliwości na insulinę insulinoopornych adipocytów 3T3-L1 przez hamowanie procesu zapalnego i poprawę przewodzenia sygnałów insulinowych, co wskazuje, że białko to może być nowym celem w zapobieganiu i leczeniu insulinooporności i cukrzycy typu 2. (Endokrynol Pol 2014; 65 (4): 253–258)
Generation of high-density high-polarization positrons via single-shot strong laser-foil interaction
We put forward a novel method for producing ultrarelativistic high-density
high-polarization positrons through a single-shot interaction of a strong laser
with a tilted solid foil. In our method, the driving laser ionizes the target,
and the emitted electrons are accelerated and subsequently generate abundant
photons via the nonlinear Compton scattering, dominated by the laser.
These photons then generate polarized positrons via the nonlinear
Breit-Wheeler process, dominated by a strong self-generated quasi-static
magnetic field . We find that placing the foil at an
appropriate angle can result in a directional orientation of , thereby polarizing positrons. Manipulating the laser polarization
direction can control the angle between the photon polarization and
, significantly enhancing the positron polarization degree.
Our spin-resolved quantum electrodynamics particle-in-cell simulations
demonstrate that employing a laser with a peak intensity of about
W/cm can obtain dense ( 10 cm) polarized positrons
with an average polarization degree of about 70\% and a yield of above 0.1 nC
per shot. Moreover, our method is feasible using currently available or
upcoming laser facilities and robust with respect to the laser and target
parameters. Such high-density high-polarization positrons hold great
significance in laboratory astrophysics, high-energy physics and new physics
beyond the Standard Model
Thermally activated delayed fluorescence materials for nondoped organic light-emitting diodes with nearly 100% exciton harvest
Funding: This study was supported by the National Natural Science Foundation of China (Nos. 52130304, 51821002, 52003185, and 52003186), the National Key Research & Development Program of China (Nos. 2020YFA0714601 and 2020YFA0714604), Suzhou Key Laboratory of Functional Nano & Soft Materials, Collaborative Innovation Center of Suzhou Nano Science & Technology, and the 111 Project.High-performance nondoped organic light-emitting diodes (OLEDs) are promising technologies for future commercial applications. Herein, we synthesized two new thermally activated delayed fluorescence (TADF) emitters that enable us, for the first time, to combine three effective approaches for enhancing the efficiency of nondoped OLEDs. First, the two emitters are designed to have high steric hindrances such that their emitting cores will be suitably isolated from those of their neighbors to minimize concentration quenching. On the other hand, each of the two emitters has two stable conformations in solid films. In their neat films, molecules with the minority conformation behave effectively as dopants in the matrix composing of the majority conformation. One hundred percent exciton harvesting is thus theoretically feasible in this unique architecture of "self-doped" neat films. Furthermore, both emitters have relatively high aspect ratios in terms of their molecular shapes. This leads to films with preferred molecular orientations enabling high populations of horizontal dipoles beneficial for optical out-coupling. With these three factors, OLEDs with nondoped emitting layers of the respective emitters both achieve nearly 100% exciton utilization and deliver over 30% external quantum efficiencies and ultralow efficiency roll-off at high brightness, which have not been observed in reported nondoped OLEDs.Publisher PDFPeer reviewe
Obesity and endocrine-related cancer: The important role of IGF-1
Obesity is increasingly becoming a global epidemic of concern and is considered a risk factor for several endocrine-related cancers. Moreover, obesity is associated with cancer development and poor prognosis. As a metabolic abnormality, obesity leads to a series of changes in insulin, IGF-1, sex hormones, IGFBPs, and adipokines. Among these factors, IGF-1 plays an important role in obesity-related endocrine cancers. This review describes the role of obesity in endocrine-related cancers, such as prostate cancer, breast cancer and pancreatic cancer, focusing on the mechanism of IGF-1 and the crosstalk with estrogen and adipokines. In addition, this review briefly introduces the current status of IGF-1R inhibitors in clinical practice and shows the prospect of IGF-1R inhibitors in combination with other anticancer drugs
Modeling Transmission of Tuberculosis with MDR and Undetected Cases
This paper presents a novel mathematical model with multidrug-resistant (MDR) and
undetected TB cases. The theoretical analysis indicates that the disease-free equilibrium is
globally asymptotically stable if R0<1; otherwise, the system may exist a locally asymptotically
stable endemic equilibrium. The model is also used to simulate and predict TB epidemic
in Guangdong. The results imply that our model is in agreement with actual data and the
undetected rate plays vital role in the TB trend. Our model also implies that TB cannot be
eradicated from population if it continues to implement current TB control strategies
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Acute Infection and Subsequent Subclinical Reactivation of Herpes Simplex Virus 2 after Vaginal Inoculation of Rhesus Macaques.
Herpes simplex virus 2 (HSV-2) is a common sexually transmitted infection with a highly variable clinical course. Many infections quickly become subclinical, with episodes of spontaneous virus reactivation. To study host-HSV-2 interactions, an animal model of subclinical HSV-2 infection is needed. In an effort to develop a relevant model, rhesus macaques (RM) were inoculated intravaginally with two or three HSV-2 strains (186, 333, and/or G) at a total dose of 1 × 107 PFU of HSV-2 per animal. Infectious HSV-2 and HSV-2 DNA were consistently shed in vaginal swabs for the first 7 to 14 days after each inoculation. Proteins associated with wound healing, innate immunity, and inflammation were significantly increased in cervical secretions immediately after HSV-2 inoculation. There was histologic evidence of acute herpesvirus pathology, including acantholysis in the squamous epithelium and ballooning degeneration of and intranuclear inclusion bodies in epithelial cells, with HSV antigen in mucosal epithelial cells and keratinocytes. Further, an intense inflammatory infiltrate was found in the cervix and vulva. Evidence of latent infection and reactivation was demonstrated by the detection of spontaneous HSV-2 shedding post-acute inoculation (102 to 103 DNA copies/swab) in 80% of RM. Further, HSV-2 DNA was detected in ganglia in most necropsied animals. HSV-2-specifc T-cell responses were detected in all animals, although antibodies to HSV-2 were detected in only 30% of the animals. Thus, HSV-2 infection of RM recapitulates many of the key features of subclinical HSV-2 infection in women but seems to be more limited, as virus shedding was undetectable more than 40 days after the last virus inoculation.IMPORTANCE Herpes simplex virus 2 (HSV-2) infects nearly 500 million persons globally, with an estimated 21 million incident cases each year, making it one of the most common sexually transmitted infections (STIs). HSV-2 is associated with increased human immunodeficiency virus type 1 (HIV-1) acquisition, and this risk does not decline with the use of antiherpes drugs. As initial acquisition of both HIV and HSV-2 infections is subclinical, study of the initial molecular interactions of the two agents requires an animal model. We found that HSV-2 can infect RM after vaginal inoculation, establish latency in the nervous system, and spontaneously reactivate; these features mimic some of the key features of HSV-2 infection in women. RM may provide an animal model to develop strategies to prevent HSV-2 acquisition and reactivation
The Controversy, Challenges, and Potential Benefits of Putative Female Germline Stem Cells Research in Mammals
The conventional view is that female mammals lose their ability to generate new germ cells after birth. However, in recent years, researchers have successfully isolated and cultured a type of germ cell from postnatal ovaries in a variety of mammalian species that have the abilities of self-proliferation and differentiation into oocytes, and this finding indicates that putative germline stem cells maybe exist in the postnatal mammalian ovaries. Herein, we review the research history and discovery of putative female germline stem cells, the concept that putative germline stem cells exist in the postnatal mammalian ovary, and the research progress, challenge, and application of putative germline stem cells in recent years
The Release of Nitric Oxide Is Involved in the β-Arrestin1-Induced Antihypertensive Effect in the Rostral Ventrolateral Medulla
β-Arrestin1 is a multifunctional scaffold protein with the ability to interact with diverse signaling molecules independent of G protein-coupled receptors. We previously reported that overexpression of β-arrestin1 in the rostral ventrolateral medulla (RVLM) decreased blood pressure (BP) and renal sympathetic nerve activity (RSNA) in spontaneously hypertensive rats (SHRs). Nitric oxide (NO) is widely reported to be involved in central cardiovascular regulation. The goal of this study was to investigate whether NO signaling contributes to the β-arrestin1-mediated antihypertensive effect in the RVLM. It was found that bilateral injection of adeno-associated virus containing Arrb1 gene (AAV-Arrb1) into the RVLM of SHRs significantly increased NO production and NO synthase (NOS) activity. Microinjection of the non-selective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME; 10 nmol) into the RVLM prevented the β-arrestin1-induced cardiovascular inhibitory effect. Furthermore, β-arrestin1 overexpression in the RVLM significantly upregulated the expression of phosphorylated neuronal NOS (nNOS) by 3.8-fold and extracellular regulated kinase 1/2 (ERK1/2) by 5.6-fold in SHRs. The β-arrestin1-induced decrease in BP and RSNA was significantly abolished by treatment with ERK1/2 small interfering RNA (ERK1/2 siRNA). Moreover, ERK1/2 siRNA attenuated the β-arrestin1-induced NO production, NOS activity, and nNOS phosphorylation in the RVLM. Taken together, these data demonstrate that the antihypertensive effect of β-arrestin1 in the RVLM is mediated by nNOS-derived NO release, which is associated with ERK1/2 activation
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