julilili42/papers huggingface dataset:
Classification of Levi degenerate homogeneous CR-manifolds in dimension 5
2008-01-01

In this context, a well-studied example of a homogeneous Levi degenerate CRmanifold is the quadratic hypersurface M := {z ∈ C 3 : (Re z 1 ) 2 +(Re z 2 ) 2 = (Re z 3 ) 2 and Re z 3 > 0}; compare, e.g., [13], [16], [23] and [31].This 5-dimensional CR-manifold has several remarkable properties and serves as motivation for various considerations in this paper.Notice that M can also be written as a tube manifoldis the future light cone in 3-dimensional space-time.A glance at this description shows that M is homogeneous under a group of complex-affine transformations.It is less obvious that the Lie algebras of global and local infinitesimal CR-transformations at a∈M, hol(M) and hol(M, a), are both isomorphic to so(2, 3), and hence have dimension 10; compare [23].Also the following 'globalization' is known: the group SO(2, 3) acts on the complex quadric Q 3 ⊂P 4 (C) by biholomorphic transformations and has a hypersurface orbit that contains M as a dense domain.The cone F clearly is a disjoint union of affine half-lines.Therefore, M is a disjoint union of complex half-planes, actually M is a fiber bundle with typical fiber H + :={z∈C:Re z >0}.However, the total space M is not even locally CR-equivalent to a product H + ×M , with M a CR-manifold.Notice that the Levi form in both cases, that is, for M and for a product of H + with a Levi nondegenerate 3-dimensional CRmanifold M , has exactly one nonzero eigenvalue at every point.Hence, one needs more invariants to distinguish those CR-manifolds.While every product C×M is holomorphically degenerate, the crucial fact here is that the light cone tube M is nondegenerate in a higher order sense: To be precise, M is 2-nondegenerate at every point, and we refer to [4] and also to [3, §11.1], for the notion of k-nondegeneracy.In the nonhomogeneous setting, for every k∈N and fixed manifold dimension it is not difficult to construct large classes of CR-manifolds, even hypersurfaces, which are k-nondegenerate at some points, but are Levi nondegenerate in a dense open subset.It seems to be much harder to construct CR-manifolds which are k-nondegenerate everywhere for k 2. Note that the CR-dimension of a homogeneous M is an upper bound for the degree k of nondegeneracy.Hence, the lowest manifold dimension for which everywhere 2-nondegenerate CR-manifolds can exist is 5.This raises the intriguing question whether, besides the light cone tube, there exist more 2-nondegenerate homogeneous CR-manifolds in dimension 5.So far, compare e.g.[14], [23], [16] and [5], all known examples in dimension 5 finally turned out to be locally CR-isomorphic to M.Even
Modulation of the Voltage-Gated Potassium Channel Kv1.5 by the SGK1 Protein Kinase Involves Inhibition of Channel Ubiquitination
2008-01-01

The serum and glucocorticoid inducible kinase SGK1 is involved in dexamethasone-induced inhibition of insulin secretion by increasing voltage-gated potassium channel (Kv) activity. SGK1 upregulates the Kv1.5 channel but the precise mechanism underlying the SGK1 dependent regulation of Kv1.5 has not been defined yet. The present study explored the signal transduction processes involved. Expression studies in Xenopus oocytes revealed that SGK1 promotes channel activity by interfering with the Nedd4-2 ubiquitination pathway, irrespective of the presence of putative SGK1 phosphorylation sites on Kv1.5. Expression of the ubiquitin ligase Nedd4-2 declined Kv1.5 currents by ubiquitinating and thereby reducing Kv1.5 plasma membrane expression. Increasing concentrations of SGK1 gradually compensated the inhibiting effect of Nedd4-2 on Kv1.5. Enhanced Kv1.5 surface abundance by SGK1 reflects decreased channel internalization as indicated by Brefeldin A experiments. In conclusion, Kv1.5 upregulation by SGK1 involves inhibition of channel ubiquitination by Nedd4-2 that leads to Kv1.5 stabilization in the plasma membrane. Our results suggest that the kinase might participate in the regulation of insulin secretion in part by controlling Kv1.5 surface abundance.
Influence of Amitriptyline on Eryptosis, Parasitemia and Survival of <i>Plasmodium Berghei</i>-Infected Mice
2008-01-01

Plasmodia express a sphingomyelinase, which is apparently required for their development. On the other hand, the sphingomyelinase product ceramide has previously been shown to delay parasite development. Moreover, ceramide triggers suicidal erythrocyte death or eryptosis, characterized by exposure of phosphatidylserine at the erythrocyte surface and cell shrinkage. Accelerated eryptosis of infected erythrocytes is considered to clear infected erythrocytes from circulating blood and, thus, to favourably influence the clinical course of malaria. The present experiments explored whether the sphingomyelinase inhibitor amitriptyline or genetic knockout of host acid sphingomyelinase influence in vitro parasite growth, eryptosis of Plasmodium falciparum-infected human erythrocytes, in vivo parasitemia and survival of P. berghei-infected mice. Phosphatidylserine exposure was determined by annexin V-binding and cell volume by forward scatter in FACS analysis. In vitro infection of human erythrocytes increased annexin- binding, an effect blunted in the presence of amitriptyline (>or=50 microM). Amitriptyline did not significantly alter intraerythrocytic parasite development but significantly (>or= 1 microM) delayed the increase in parasitemia in vitro. Most importantly, amitriptyline treatment (1 mM in drinking water) resulted in a significant delay of parasitemia and death of infected mice. However, upon infection, ceramide formation was stimulated in both, acid sphingomyelinase knockout mice (Smpd1(-/-)) and their wild type littermates (Smpd1(+/+)). Parasitemia following P. berghei infection was significantly lower in Smpd1(-/-) than in Smpd1(+/+) mice but did not significantly extend the life span of infected animals. In conclusion, mammalian and parasite sphingomyelinase contribute to ceramide formation during malaria, whereby the parasite sphingomyelinase ultimately determines the course of the infection. Amitriptyline presumably blocks both sphingomyelinases and, thus, its use might be a novel strategy to treat malaria.
Tighter multipole-based integral estimates and parallel implementation of linear-scaling AO–MP2 theory
2008-01-01

Within an atomic-orbital-based (AO-based) formulation of second-order Møller-Plesset perturbation theory (MP2), we present a novel screening procedure which allows us to preselect numerically significant two-electron integrals more efficiently, especially for large basis sets. The screening is based on our recently introduced multipole-based integral estimates (MBIE) method [J. Chem. Phys., 2005, 123, 184102], that allows to exploit the 1/R(4) or 1/R(6) coupling between electronic charge distributions in transformed integral products within AO-MP2. In this way, linear scaling is attained with fully-controlled numerical accuracy. Furthermore, a parallel implementation of our linear-scaling AO-MP2 method is described, which also allows us to perform calculations with larger basis sets. First calculations reveal that for e.g. linear alkanes the scaling of the number of required transformed integral products is almost equal for 6-31G* and cc-pVTZ basis sets. Using the improved MBIE screening, the largest parallel calculation was performed for a ribozyme fragment consisting of 497 atoms and 5697 basis functions, while our largest AO-MP2 calculation was performed for a stacked DNA system (16 base pairs) comprising 1052 atoms and 10 674 basis functions on a single processor.
Diagnosing meaning errors in short answers to reading comprehension questions
2008-01-01

A common focus of systems in Intelligent Computer-Assisted Language Learning (ICALL) is to provide immediate feedback to language learners working on exercises. Most of this research has focused on providing feedback on the form of the learner input. Foreign language practice and second language acquisition research, on the other hand, emphasizes the importance of exercises that require the learner to manipulate meaning.
A CRITICAL VIEW OF THE EVIDENCE FOR A SOUTHERN AFRICAN ORIGIN OF BEHAVIOURAL MODERNITY
2008-01-01

The Middle Stone Age of southern Africa has produced a wealth of new data that points to this region as a centre for cultural development during the Middle and Late Pleistocene. In South Africa it has become scientifically fashionable and politically expedient in recent years to emphasize these important findings and to suggest that southern Africa represents the source of behavioural modernity. While a case can be made for this point of view, this paper examines the strengths and weaknesses of this hypothesis and ultimately rejects the idea of a monocentric southern African origin in favour of a model for a histori-cally contextualized, polycentric rise of cultural modernity. This model for Mosaic Polycentric Modernity (MPM), while not denying the unique role of Africa in the later phases of human evolution, better matches the global archaeological record than the models emphasizing strictly African origins.
Cox Rings and Combinatorics II
2008-01-01

We study varieties with a finitely generated Cox ring.In a first part, we generalize a combinatorial approach developed in earlier work for varieties with a torsion free divisor class group to the case of torsion.Then we turn to modifications, e.g., blow ups, and the question how the Cox ring changes under such maps.We answer this question for a certain class of modifications induced from modifications of ambient toric varieties.Moreover, we show that every variety with finitely generated Cox ring can be explicitly constructed in a finite series of toric ambient modifications from a combinatorially minimal one.
PGK1 a Potential Marker for Peritoneal Dissemination in Gastric Cancer
2008-01-01

The overexpression of PGK1 and its signalling targets may be a expression-pathway in diffuse primary gastric carcinomas promoting peritoneal dissemination and may function as prognostic markers and/or be potential therapeutic targets to prevent the migration of gastric carcinoma cells into the peritoneum.
Association of SGK1 Gene Polymorphisms with Type 2 Diabetes
2008-01-01

The serum and glucocorticoid inducible kinase SGK1 is genomically upregulated by glucocorticoids and in turn stimulates a variety of carriers and channels including the renal epithelial Na(+) channel ENaC and the intestinal Na(+) glucose transporter SGLT1. Twin studies disclosed an association of a specific SGK1 haplotype with moderately enhanced blood pressure in individuals who are carrying simultaneously a homozygous genotype for a variant in intron 6 [I6CC] and a homozygous or heterozygous genotype for the C allele of a polymorphism in exon 8 [E8CC/CT] of the SGK1 gene. A subsequent study confirmed the impact of this risk haplotype on blood pressure. SGK1 knockout mice are resistant to the insulin and high salt induced increase of blood pressure, glucocorticoid induced increase of electrogenic glucose transport, and glucocorticoid induced suppression of insulin release. The present study explored whether the I6CC/E8CC/CT haplotype impacts on the prevalence of type 2 diabetes. The prevalence of the I6CC genotype was 3.1% in a healthy German, 2.4 % in a healthy Romanian and 11.6 % in a healthy African population from Ghana (p=0.0006 versus prevalence in Caucasians). Comparison of genotype frequencies between type 2 diabetic patients and the respective control groups revealed significant differences for the intron 6 T>C variant. Carriers of at least one T allele were protected against type 2 diabetes (Romanians: p=0.023; OR 0.29; 95% CI 0.09-0.89; Germans: p=0.01; OR 0.37; 95% CI 0.17-0.81). The SGK1 risk haplotype (I6CC/E8CC/CT) was significantly (p=0.032; OR 4.31, 95% CI 1.19-15.58) more frequent in diabetic patients (7.2 %) than in healthy volunteers from Romania (1.8%). The observations support the view that SGK-1 may participate in the pathogenesis of metabolic syndrome.
RESERVOIR POTENTIAL OF A LACUSTRINE MIXED CARBONATE / SILICICLASTIC GAS RESERVOIR: THE LOWER TRIASSIC ROGENSTEIN IN THE NETHERLANDS
2008-01-01

The Lower Triassic Rogenstein Member of the Buntsandstein Formation produces gas at the De Wijk and Wanneperveen fields, NE Netherlands and consists mainly of claystones with intercalated oolitic limestone beds. The excellent reservoir properties of the oolites (φ= 20‐30%; k = 5‐4000 mD) are predominantly controlled by depositional facies. Oolitic limestones are interpreted as the storm and wave deposits of a shallow, desert lake located in the Central European Buntsandstein Basin. The vertical sequence of lithofacies in the Rogenstein Member indicates cyclic changes of relative lake level. The reservoir rock is vertically arranged in a three‐fold hierarchy of cycles, recognised both in cores and wireline logs. These cycles are a key to understanding the distribution of reservoir facies, and are used as the basis for a high‐resolution sequence stratigraphic correlation of the reservoir units. Slight regional‐scale thickness variations of the Rogenstein Member (in the order of tens of metres) are interpreted as the effects of differential subsidence associated with the inherited Palaeozoic structural framework. The depositional basin can be subdivided into subtle palaeo‐highs and ‐lows which controlled facies distribution during Rogenstein deposition. Oolitic limestones show their greatest lateral extent and thickest development in the Middle Rogenstein during large‐scale maximum flooding. Potential reservoir rocks (decimetre to metres thick) are present in the NE Netherlands, in particular in the Lauwerszee Trough and the Lower Saxony Basin, where abundant gas shows of 200 ‐ 4000 ppm CH 4 have been recorded. Preserved primary porosity is interpreted to be a result of rapid burial in subtle depositional palaeo‐lows in this area. The thickest, amalgamated oolite intervals (tens of metres thick) occur in the eastern part of the Central Netherlands Basin. Because of poor reservoir properties, other areas appear to be less promising in terms of Rogenstein exploration potential.
Crohn’s disease-Defect in innate defence
2008-01-01

Crohn's disease may principally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is complex, the likely primary defect lies in the innate rather than adaptive immunity, particularly in the chemical antimicrobial barrier of the mucosa. Crohn's ileitis is associated with a reduced expression of the Wnt signalling pathway transcription factor T-cell factor 4 (TCF4), which is regulating Paneth cell differentiation. As a result, the alpha-defensins and principal Paneth cell products HD5 and HD6 are deficiently expressed in ileal disease, independent of current inflammation. In contrast, Crohn's colitis is typically associated with an impaired induction of the beta-defensins HBD2 and HBD3 caused by fewer gene copy numbers in the gene locus of the beta-defensins on chromosome 8. This ileal and colonic defect in innate defence mediated by a deficiency of the protective alpha- and beta-defensins may enable the luminal microbes to invade the mucosa and trigger the inflammation. A better understanding of the exact molecular mechanisms behind ileal and colonic Crohn's disease may give rise to new therapeutic strategies based on a stimulation of the protective innate immune system.
BART
2008-01-01

Developing a full coreference system able to run all the way from raw text to semantic interpretation is a considerable engineering effort, yet there is very limited availability of off-the shelf tools for researchers whose interests are not in coreference, or for researchers who want to concentrate on a specific aspect of the problem. We present BART, a highly modular toolkit for developing coreference applications. In the Johns Hopkins workshop on using lexical and encyclopedic knowledge for entity disambiguation, the toolkit was used to extend a reimplementation of the Soon et al. (2001) proposal with a variety of additional syntactic and knowledge-based features, and experiment with alternative resolution processes, preprocessing tools, and classifiers.
A Role of Ion Channels in the Endothelium-Independent Relaxation of Rat Mesenteric Artery Induced by Resveratrol
2008-01-01

Recently it has been suggested that resveratrol relaxes different isolated arteries. The present study addressed the question whether different ion channels are involved in the endothelium-independent mechanism of vasodilatation induced by resveratrol. For that purpose, we tested the action of resveratrol on the rat mesenteric artery without endothelium. Resveratrol induced concentration-dependent relaxation of rat mesenteric artery. Among the K(+)-channel blockers, 4-amynopiridine (4-AP) moderately antagonized the resveratrol-induced relaxation, while glibenclamide, tetraethylammonium chloride, charybdotoxin, margatoxin, and barium chloride did not inhibit resveratrol-induced vasorelaxation. In rings, precontracted with 100 mM K(+), the relaxant responses to resveratrol were highly significantly shifted to the right compared to those obtained in rings precontracted with phenylephrine, but resveratrol-induced maximal relaxation was only slightly affected. In order to minimize the influence of K(+) channels and voltage-gated Ca(2+) channels (VGCCs) in vascular smooth muscle, the third contraction was made by 100 mM K(+) in the presence of nifedipine. The relaxant response to resveratrol was abolished. Thus, the mechanism of vasorelaxation induced by resveratrol probably involves activation of 4-AP-sensitive K(+) channels. Its ability to completely relax the mesenteric artery precontracted with K(+)-rich solution suggests that K(+) channel-independent mechanism(s) are involved in its vasorelaxant effect. It seems that interaction with VGCCs plays a part in this K(+) channel-independent effect of resveratrol.
Phosphatidylinositide Dependent Kinase Deficiency Increases Anxiety and Decreases GABA and Serotonin Abundance in the Amygdala
2008-01-01

Pathological anxiety is paralleled by deficits in serotonergic and GABAergic neurotransmission in the amygdala. Conversely, anxiety disorders and depression may be reversed by brain-derived neurotrophic factor (BDNF). BDNF signaling involves Phosphatidylinositol 3-Kinase / 3-phosphoinositide-dependent protein kinase 1 (PI3K/PDK1). We thus hypothesized that impaired function of PDK1 might be associated with increased anxiety and concomitant neurotransmitter changes. Here we used the hypomorphic PDK1(hm) mouse to investigate anxiety behavior in different settings: PDK1(hm) mice differed from Wt littermates PDK1(WT) in several behavioral measures related to anxiety and exploration, namely in the open field, dark-light box, O-maze and startle response. Further we analyzed the brain substrate underlying this phenotype and found significantly decreased GABA, taurine and serotonin concentrations in the amygdala and olfactory bulb of PDK1(hm) mice, while BDNF and nerve growth factor (NGF) concentrations were not significantly different between PDK1(hm) and PDK1(WT) mice. These results suggest that impaired PI3K signaling in the PDK1(hm) mouse reduces concentrations of GABA and serotonin in anxiety related brain regions and can serve as a molecular substrate for behavior indicative for anxious and depressive-like mood states.
General functions to transform associate data to host data, and their use in phylogenetic inference from sequences with intra-individual variability
2008-01-01

Because of their generality, the transformation functions may be applied to a wide range of biological problems that are interpretable in terms of hosts and associates. Regarding cloned sequences, the formulae have a high potential to accurately reflect evolutionary relationships within angiosperm genera, and to identify hybrids and ancestral taxa. These results corroborate earlier ones which showed that treelikeness measures are a valuable tool in comparative studies of biological distance functions.
Angiogenesis: The New Potential Target for the Therapy of Psoriasis?
2008-01-01

Angiogenesis is a hallmark of chronic inflammation such as psoriasis. Unraveling the pathogenesis of psoriasis shows that several proangiogenic mediators are activated and highly expressed during psoriasis. Vascular endothelial growth factor, hypoxia- inducible factor, tumor necrosis factor, interleukin-8 and angiopoietins are considered to be the main players responsible for the strong vessel formation in psoriasis. The proangiogenic milieu in the skin seems to result from a proinflammatory immune response initiated by T helper cells. Interestingly, several small molecules as well as modern biologics used for systemic therapy of psoriasis have been shown to provide not only immune regulatory effects but also influence endothelial cell biology. Thus, direct targeting of angiogenesis may not only help to understand psoriasis pathogenesis but also to develop new strategies to treat psoriasis with therapeutics that halt the angiogenesis required for the inflammatory disease.
Activation of PI3K Is Associated with Reduced Survival in Renal Cell Carcinoma
2008-01-01

&lt;i&gt;Objectives:&lt;/i&gt; The epidermal growth factor receptor- (EGFR) activated phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/Akt) pathway is associated with tumorigenesis and progression. The aims of the present study were to determine the expression patterns of Akt pathway parameters PI3K, phosphatase and tensin homolog (PTEN), phosphor-Akt (p-Akt) and their combination, for their possible prognostic value in renal cell carcinoma (RCC). PTEN dephosphorylates the liquid product of PI3K. &lt;i&gt;Methods:&lt;/i&gt; Tumor samples from 176 RCC patients were investigated for PTEN, p-Akt and PI3K expression by immunohistochemistry. Expression levels were correlated to clinical variables and postoperative outcome by uni- and multivariate statistical analysis. &lt;i&gt;Results:&lt;/i&gt; The various expression levels within the tumor samples were independent of histological grade and tumor stage, due to different levels of activation of the PI3K/p-Akt pathway. The activation of PI3K protein was found to be significantly associated with reduced survival times (p = 0.0304, multivariate analysis). Analysis of combined biomarker expressions showed that decreased long-term survival was correlated with PTEN low/p-Akt high expression (p &lt; 0.05). &lt;i&gt;Conclusions:&lt;/i&gt; Activation of the PI3K pathway is significantly associated with adverse clinical outcome in RCC. Analysis of biomarker combinations might identify high-risk patients and a subsequent need to adapt treatment modalities. Molecular pathways regulating PI3K activation appear to be promising targets for drug development in the clinical management of RCC patients.