1,084 research outputs found
data Hegemann et al 2017 FrontZool
No full textAll data for the publication "Hegemann A, Pardal S & Matson KD: Indices of immune function used by ecologists are mostly unaffected by repeated freeze-thaw cycles and methodological deviations. Frontiers in Zoology 14:43" divided over 4 different sheet
Native PAGE experiments on SL1-wt RNA kissing dimer (KD) in the presence of sub-stoichiometric amounts of NCp7, run in the TBE buffer
No full text<p><b>Copyright information:</b></p><p>Taken from "Nucleocapsid protein-mediated maturation of dimer initiation complex of full-length SL1 stemloop of HIV-1: sequence effects and mechanism of RNA refolding"</p><p></p><p>Nucleic Acids Research 2007;35(6):2026-2034.</p><p>Published online 6 Mar 2007</p><p>PMCID:PMC1874624.</p><p>© 2007 The Author(s)</p> KD of SL1-wt was incubated with NCp7 at ambient temperature for 18 h in the RNA strand-to-protein ratio of 2:0, 2:2, 2:1.6, 2:0.8, 2:0.4 and 2:0.2, as indicated. The upper band in each lane (‘LD’) corresponds to mature linear dimer, while the lower monomer band (‘M’) emanates from the residual KD that dissociates during PAGE in the TBE buffer. Increasing intensity of the monomer band and simultaneous decrease in the dimer band across the lanes correlates with the amount of NCp7 present in each complex
Therapeutic studies in hepatic encephalopathy
No full textThis article has arisen from presentations made at the 4th International Hannover Conference on Hepatic Encephalopathy held in Dresden, 2006. Each author as listed describes their presentation given as part of a section entitled "Therapeutic Studies in Hepatic Encephalopathy." The first section deals with the justification for placebo-controlled trials in hepatic encephalopathy. The other two sections discuss, in detail, outcome parameters for therapeutic studies in the clinical and research setting, respectivel
Concurrent linearizable nearest neighbour search in lockfree-kd-Tree
No full textThe Nearest neighbour search (NNS) is a fundamental problem in many application domains dealing with multidimensional data. In a concurrent setting, where dynamic modi-fications are allowed, a linearizable implementation of NNS is highly desirable. This paper introduces the LockFree-kD-Tree (LFkD-Tree): A lock-free concurrent kD-Tree, which implements an abstract data type (ADT) that provides the operations Add, Remove, Contains, and NNS. Our implementation is linearizable. The operations in the LFkD-Tree use single-word read and compare-And-swap (CAS) atomic primitives, which are readily supported on available multi-core processors. We experimentally evaluate the LFkD-Tree using several benchmarks comprising real-world and synthetic datasets. The experiments show that the presented design is scalable and achieves signi cant speed-up compared to the implementations of an existing sequential kD-Tree and a recently proposed multidimensional indexing structure, PH-Tree.\ua0\ua9 2018 Copyright held by the owner/author(s)
Dispersive to nondispersive transition in the plane wake and channel flows
No full textBy varying the wavenumber over a large and finely discretized interval of values, we analyse the phase and group velocity of linear three-dimensional travelling waves both in the plane wake and channel flows to get the transition between dispersive and non-dispersive behaviour. The dispersion relation is computed from the Orr-Sommerfeld and Squire eigenvalue problem by observing the least stable mode, see figure 2, panels (a,b) and the comparison with [1, 2, 4–11, 15, 16]. The group velocity vg is also shown. The Reynolds number varies in the 20-100, 1000-8000 ranges for the wake and the channel flow, respectively, while we consider wavenumbers in the range 0.1-10. The wake basic flow consists of the first two orders of the Navier-Stokes matched asymptotic expansion described in [3, 13, 14]. At low wavenumbers we observe a dispersive behaviour where the phase speed and the group velocity substantially differ. The relevant perturbed solution is amenable to the typical solution belonging to the left branch of the eigenvalue spectrum, see the two examples shown in figure 1 (channel flow: Re = 6000; k = 1; wake Re = 100; k = 0:7). By rising the wave number value, we observe a sharp transition from the dispersive to the nondispersive regime. This transition is located at a critical wave number kd which is a function of the Reynolds number Re, the wave angle _, and the wake downstream observation point x0. Precisely, kd increases with Re and decreases with _ for the wake flow, while these trends are reversed for the channel flow, see tables 1,2. Beyond the wavenumber threshold, the observed least-stable mode belongs to the right branch of the spectrum. The asymptotic solutions in the dispersive region are wall modes for the channel flow , and in-wake modes for the wake flow. This means that, for both the flows, the dispersive behaviour is related to perturbations with high momentum variations (high vorticity) in correspondence to the base flow high-shear region. On the contrary, if k > kd the solutions are central modes for the channel case, and out-of-wake modes for the wake flow. In these cases, the disturbance has high variations outside the base flow high-shear region. To understand the physical mechanism of the dispersive-nondispersive transition we focused on time variation of the wave kinetic energy associated to the convective transport. Figure 2 (c,d) shows the convective term as a function of the wavenumber for the two least stable modes. We observe that the dispersive-nondisperive transition allows waves k > kd to keep the lowest possible temporal variation of kinetic energy, i.e. the lowest decay. This remains true also when all the other more stable modes are considered. In practice nondispersive waves maintain their convective energy with k
The Ketogenic Diet Alters the Hypoxic Response and Affects Expression of Proteins Associated with Angiogenesis, Invasive Potential and Vascular Permeability in a Mouse Glioma Model
No full textabstract: Background
The successful treatment of malignant gliomas remains a challenge despite the current standard of care, which consists of surgery, radiation and temozolomide. Advances in the survival of brain cancer patients require the design of new therapeutic approaches that take advantage of common phenotypes such as the altered metabolism found in cancer cells. It has therefore been postulated that the high-fat, low-carbohydrate, adequate protein ketogenic diet (KD) may be useful in the treatment of brain tumors. We have demonstrated that the KD enhances survival and potentiates standard therapy in a mouse model of malignant glioma, yet the mechanisms are not fully understood.
Methods
To explore the effects of the KD on various aspects of tumor growth and progression, we used the immunocompetent, syngeneic GL261-Luc2 mouse model of malignant glioma.
Results
Tumors from animals maintained on KD showed reduced expression of the hypoxia marker carbonic anhydrase 9, hypoxia inducible factor 1-alpha, and decreased activation of nuclear factor kappa B. Additionally, tumors from animals maintained on KD had reduced tumor microvasculature and decreased expression of vascular endothelial growth factor receptor 2, matrix metalloproteinase-2 and vimentin. Peritumoral edema was significantly reduced in animals fed the KD and protein analyses showed altered expression of zona occludens-1 and aquaporin-4.
Conclusions
The KD directly or indirectly alters the expression of several proteins involved in malignant progression and may be a useful tool for the treatment of gliomas.The article is published at http://journals.plos.org/plosone/article?id=10.1371/journal.pone.013035
Discrete spectra for confined and unconfined-a/r+ br^ 2 potentials in d dimensions
No full textSource type: Electronic(1
Author response
No full textMissense mutations in ATM kinase, a master regulator of DNA damage responses, are found in many cancers, but their impact on ATM function and implications for cancer therapy are largely unknown. Here we report that 72% of cancer-associated ATM mutations are missense mutations that are enriched around the kinase domain. Expression of kinase-dead ATM (Atm(KD/-)) is more oncogenic than loss of ATM (Atm(-/-)) in mouse models, leading to earlier and more frequent lymphomas with Pten deletions. Kinase-dead ATM protein (Atm-KD), but not loss of ATM (Atm-null), prevents replication-dependent removal of Topo-isomerase I-DNA adducts at the step of strand cleavage, leading to severe genomic instability and hypersensitivity to Topo-isomerase I inhibitors. Correspondingly, Topo-isomerase I inhibitors effectively and preferentially eliminate Atm(KD/-), but not Atm-proficientor Atm(-/-) leukemia in animal models. These findings identify ATM kinase-domain missense mutations as a potent oncogenic event and a biomarker for Topo-isomerase I inhibitor based therapy
Spectral characteristics for a spherically confined- a/r+ br2 potential
No full textSource type: Electronic(1
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