141 research outputs found

    Extremely Inclined Orbit of S-type Planet γ\gamma Cep Ab Induced by Eccentric Kozai-Lidov Mechanism

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    γ\gamma Cep Ab is a typical S-type planet, which occupies a nearly perpendicular planetary orbit relative to the binary. Here we use the Markov Chain Monte Carlo (MCMC) sampler to conduct full N-body fitting and derive self-consistent orbital solutions for this hierarchical system. Then we employ the Eccentric Kozai-Lidov (EKL) mechanism to explain the extremely inclined orbit of S-type planet γ\gamma Cep Ab. The EKL mechanism plays an essential role in exploring significant oscillations of the mutual inclination imuti_{\mathrm{mut}} between the planet and the secondary star. We perform qualitative analysis and extensive numerical integrations to investigate the flip conditions and timescales of γ\gamma Cep Ab's orbit. When the planetary mass is 15 MJupM_{\mathrm{Jup}}, the planet can reach imut∼i_{\mathrm{mut}} \sim 113∘^{\circ} with the critical initial conditions of imut<60∘i_{\mathrm{mut}} < 60^{\circ} and e1<0.7e_1<0.7. The timescale for the first orbital flip decreases with the increase of the perturbation Hamiltonian. Flipping orbits of γ\gamma Cep Ab are confirmed to have a large possibility to retain stable based on surfaces of section and the secular stability criterion. Furthermore, we extend the application of EKL to general S-type planetary systems with a1/a2≤0.1a_1/a_2\leq0.1, where the most intense excitation of imuti_{\mathrm{mut}} occurs when a1/a2=0.1a_1/a_2=0.1 and e2∼0.8e_2 \sim 0.8, and the variation of planetary mass mainly affect the flip possibility where e1≤0.3e_1\leq 0.3.Comment: 21 pages, 14 figures, accepted for publication in A

    Demand Shaping to Achieve Steady Electricity Consumption with Load Balancing in a Smart Grid

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    The purpose of this paper is to study conflicting objectives between the grid operator and consumers in a future smart grid. Traditionally, customers in electricity grids have different demand profiles and it is generally assumed that the grid has to match and satisfy the demand profiles of all its users. However, for system operators and electricity producers, it is usually most desirable, convenient and cost effective to keep electricity production at a constant rate. The temporal variability of electricity demand forces power generators, especially load following and peaking plants to constantly manipulate electricity production away from a steady operating point

    Vernier Ring Based Pre-bond Through Silicon Vias Test in 3D ICs

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    Defects in TSV will lead to variations in the propagation delay of the net connected to the faulty TSV. A non-invasive Vernier Ring based method for TSV pre-bond testing is proposed to detect resistive open and leakage faults. TSVs are used as capacitive loads of their driving gates, then time interval compared with the fault-free TSVs will be detected. The time interval can be detected with picosecond level resolution, and digitized into a digital code to compare with an expected value of fault-free. Experiments on fault detection are presented through HSPICE simulations using realistic models for a 45 nm CMOS technology. The results show the effectiveness in the detection of time interval 10 ps, resistive open defects 0.2 kΩ above and equivalent leakage resistance less than 18 MΩ. Compared with existing methods, detection precision, area overhead, and test time are effectively improved, furthermore, the fault degree can be digitalized into digital code

    Nudel functions in membrane traffic mainly through association with Lis1 and cytoplasmic dynein

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    Nudel and Lis1 appear to regulate cytoplasmic dynein in neuronal migration and mitosis through direct interactions. However, whether or not they regulate other functions of dynein remains elusive. Herein, overexpression of a Nudel mutant defective in association with either Lis1 or dynein heavy chain is shown to cause dispersions of membranous organelles whose trafficking depends on dynein. In contrast, the wild-type Nudel and the double mutant that binds to neither protein are much less effective. Time-lapse microscopy for lysosomes reveals significant reduction in both frequencies and velocities of their minus end–directed motions in cells expressing the dynein-binding defective mutant, whereas neither the durations of movement nor the plus end–directed motility is considerably altered. Moreover, silencing Nudel expression by RNA interference results in Golgi apparatus fragmentation and cell death. Together, it is concluded that Nudel is critical for dynein motor activity in membrane transport and possibly other cellular activities through interactions with both Lis1 and dynein heavy chain

    Teamwork Makes the Dream Work: Purdue\u27s IMPACT Course Transformation Faculty Learning Community

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    Describes the collaborative faculty learning community established within a specific IMPACT team from the Spring 2017 Cohort. Describes the IMPACT course redesign program and experiences of the individual faculty fellows working within the team to redesign their courses

    Teamwork Makes the Dream Work: Purdue\u27s IMPACT Course Transformation Faculty Learning Community

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    Describes the collaborative faculty learning community established within a specific IMPACT team from the Spring 2017 Cohort. Describes the IMPACT course redesign program and experiences of the individual faculty fellows working within the team to redesign their courses

    Involvement of Human Papillomaviruses in Cervical Cancer

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    Human papillomaviruses (HPV) are the first viruses to have been acknowledged to prompt carcinogenesis, and they are linked with cancers of the uterine cervix, anogenital tumors, and head and neck malignancies. This paper examines the structure and primary genomic attributes of HPV and highlights the clinical participation of the primary HPV serotypes, focusing on the roles that HPV-16 and 18 play in carcinogenesis. The mechanisms that take place in the progression of cervical neoplasia are described. The oncogenic proteins E6 and E7 disrupt control of the cell cycle by their communication with p53 and retinoblastoma protein. Epidemiological factors, diagnostic tools, and management of the disease are examined in this manuscript, as are the vaccines currently marketed to protect against viral infection. We offer insights into ongoing research on the roles that oxidative stress and microRNAs play in cervical carcinogenesis since such studies may lead to novel methods of diagnosis and treatment. Several of these topics are surfacing as being critical for future study. One particular area of importance is the study of the mechanisms involved in the modulation of infection and cancer development at cervical sites. HPV-induced cancers may be vulnerable to immune therapy, offering the chance to treat advanced cervical disease. We propose that oxidative stress, mRNA, and the mechanisms of HPV infection will be critical points for HPV cancer research over the next decade

    Deciphering the mechanism of PSORI-CM02 in suppressing keratinocyte proliferation through the mTOR/HK2/glycolysis axis

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    Hyperplasia of epidermal keratinocytes that depend on glycolysis is a new hallmark of psoriasis pathogenesis. Our previous studies demonstrated that PSORI-CM02 could halt the pathological progression of psoriasis by targeting inflammatory response and angiogenesis, but its effect(s) and mechanism(s) on proliferating keratinocytes remained unclear. In this study, we aim to identify components of PSORI-CM02 that are absorbed into the blood and to determine the effect(s) of PSORI-CM02 on keratinocyte proliferation and its molecular mechanism(s). We used the immortalized human epidermal keratinocyte cell line, HaCaT, as an in vitro model of proliferating keratinocytes and the imiquimod-induced psoriasis mouse (IMQ) as an in vivo model. Metabolite profiles of vehicle pharmaceutic serum (VPS), PSORI-CM02 pharmaceutic serum (PPS), and water extraction (PWE) were compared, and 23 components of PSORI-CM02 were identified that were absorbed into the blood of mice. Both PPS and PWE inhibited the proliferation of HaCaT cells and consequently reduced the expression of the proliferation marker ki67. Additionally, PPS and PWE reduced phosphorylation levels of mTOR pathway kinases. Seahorse experiments demonstrated that PPS significantly inhibited glycolysis, glycolytic capacity, and mitochondrial respiration, thus reducing ATP production in HaCaT cells. Upon treatments of PPS or PWE, hexokinase 2 (HK2) expression was significantly decreased, as observed from the set of glycolytic genes we screened. Finally, in the IMQ model, we observed that treatment with PSORI-CM02 or BPTES, an inhibitor of mTOR signaling, reduced hyperproliferation of epidermal keratinocytes, inhibited the expression of p-S6 and reduced the number of proliferating cell nuclear antigen (PCNA)-positive cells in lesioned skin. Taken together, we demonstrate that PSORI-CM02 has an anti-proliferative effect on psoriatic keratinocytes, at least in part, by inhibiting the mTOR/HK2/glycolysis axis
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