julilili42/papers huggingface dataset:
Exploiting parallelism in physically-based simulations on multi-core processor architectures
2007-05-20

As multi-core processor systems become more and more widespread, the demand for designing efficient parallel algorithms propagates also into the field of computer graphics. This is especially true for the physically-based simulation, which is notorious for expensive numerical methods. In this paper we explore possibilities for accelerating these algorithms on modern multi-core architectures. As an application we focus on physically-based cloth simulation. In this context, two distinct problems can be identified: the physical model and the collision handling stage — both bearing potential bottlenecks for the simulation. From the parallelization point of view these two components are substantially different. The physical model can be treated efficiently using static problem decomposition. The collision handling problem, however, requires a different approach, due to its dynamically changing structure. We address this problem using multi-threaded programming with fully dynamic task decomposition. Furthermore, we propose a new task splitting approach based on a robust work estimate. The associated data is derived from temporal coherence. Altogether, the combination of different parallelization techniques leads to a concise and yet versatile framework for highly efficient physical simulation.
Sentinel Lymph Node Biopsy in Colon Cancer
2007-05-21

The contribution of SLNB to conventional nodal staging of colon cancer patients is still unspecified. Technical problems have to be resolved before a definite conclusion can be drawn in this regard. However, SLNB identifies about one fourth of stage II patients to reveal MM/ITC in lymph nodes. Further studies must clarify the clinical impact of these findings in terms of prognosis and the indication of adjuvant therapy.
A novel LRRK2 mutation in an Austrian cohort of patients with Parkinson's disease
2007-05-21

Abstract To investigate the frequency of mutations in the Leucine‐Rich Repeat Kinase 2 gene ( LRRK2 ) in a sample of Austrian Parkinson's disease (PD) patients, we sequenced the complete coding region in 16 patients with autosomal dominant PD. Furthermore, we sequenced exons 31, 35, and 41 additionally in 146 patients with idiopathic PD and 30 patients with dementia with Lewy bodies. Furthermore, all 192 patients were screened for 21 putative LRRK2 mutations. While the most common mutation G2019S and the risk variant G2385R were not found in our samples, we detected a novel missense mutation (S973N) in a patient with familial, late‐onset and dopa‐responsive PD. © 2007 Movement Disorder Society
Reduced coherence in double-slit diffraction of neutrons
2007-05-21

In diffraction experiments with particle beams, several effects lead to a fringe visibility reduction of the interference pattern. We theoretically describe the intensity one can measure in a double-slit setup and compare the results with the experimental data obtained with cold neutrons. Our conclusion is that for cold neutrons the fringe visibility reduction is due not to decoherence, but to initial incoherence.
Implicit learning, executive function and hedonic activity in chronic polydrug abusers, currently abstinent polydrug abusers and controls
2007-05-22

ABSTRACT Aims The study seeks to evaluate impairments of implicit learning and executive function in chronic polydrug abusers. It was hypothesized that implicit learning and executive function correlate with anhedonia. Design A cross‐sectional group comparison. Settings Department of Psychiatry, University of Tübingen, Germany. Participants A total of 25 male polydrug abusers with opiate dependence, n = 26 polydrug abusers abstinent for more than 3 months and n = 26 non‐drug‐using healthy males. Setting Abstinent polydrug abusers were recruited from a community treatment centre, current polydrug abusers from local drug counselling services and controls through advertisements. Measurements A psychological battery assessing implicit learning (serial reaction‐time task), various executive functions (latent inhibition, delayed matching‐to‐sample, Trail Making Test, acquisition and modification of conditioned responses, figural reasoning) and verbal logic memory was administered. Hedonic thoughts and activities as well as depressive symptoms were assessed through questionnaires. Findings In chronic polydrug abusers, there were moderate impairments of implicit learning, of acquisition, reversal and extinction of conditioned responses, of latent inhibition as well as anhedonia, while working memory was spared. In the abstinent group, cognitive performance was normal except for latent inhibition and more anhedonia and depression than in controls. Conclusions The findings suggest that current polydrug abusers suffer from impairment of many cognitive functions and from anhedonia. During abstinence, there is near normal cognitive function but still anhedonia. Anhedonia was correlated with implicit learning but not with executive function.
A soluble, magnesium‐independent prenyltransferase catalyzes reverse and regular C‐prenylations and O‐prenylations of aromatic substrates
2007-05-22

Fnq26 from Streptomyces cinnamonensis DSM 1042 is a new member of the recently identified CloQ/Orf2 class of prenyltransferases. The enzyme was overexpressed in E. coli and purified to apparent homogeneity, resulting in a soluble, monomeric protein of 33.2 kDa. The catalytic activity of Fnq26 is independent of the presence of Mg 2+ or other divalent metal ions. With flaviolin (2,5,7‐trihydroxy‐1,4‐naphthoquinone) as substrate, Fnq26 catalyzes the formation of a carbon–carbon‐bond between C‐3 (rather than C‐1) of geranyl diphosphate and C‐3 of flaviolin, i.e. an unusual “reverse” prenylation. With 1,3‐dihydroxynaphthalene and 4‐hydroxybenzoate as substrates Fnq26 catalyzes O ‐prenylations.
Magnetic resonance imaging to assess acute changes in atrial and ventricular parameters after transcatheter closure of atrial septal defects
2007-05-22

Abstract Purpose To evaluate acute changes in atrial and ventricular parameters by the use of cardiac magnetic resonance imaging (MRI) in patients with percutaneous transcatheter atrial septal defects (ASD) closure. Materials and Methods The study included 14 patients (six males and eight females, 45 ± 18 years) with congenital ASD. Cardiac MRI (1.5T Philips Intera CV) was performed before and within 24 hours after transcatheter ASD closure. Right atrial (RA) and left atrial (LA) dimensions, as well as right (RV) and left (LV) ventricular end‐diastolic (ED) volumes were determined. Atrial size was assessed by planimetry of the maximum RA and LA areas in a standard four‐chamber view, and ventricular volumes were calculated according to a modified Simpson's rule in short‐axis views. Results The mean RA decreased significantly from 27.6 ± 6.4 cm 2 before closure to 24.4 ± 5.6 cm 2 after the procedure ( P = 0.0018), whereas the LA area did not change (24.1 ± 4.7 cm 2 vs. 23.8 ± 5.2 cm 2 , P = 0.76). The RV volumes, volume index, and ejection fraction (EF) decreased significantly from 229 ± 64 mL to 181 ± 43 mL ( P &lt; 0.001, average reduction = 19% ± 15%), from 126.0 ± 37.2 mL/m 2 to 96.6 ± 28.6 mL/m 2 ( P &lt; 0.0001) and from 64 ± 5% to 58% ± 7% ( P = 0.01), respectively. The LV volumes and volume index remained unchanged (114 ± 25 mL vs. 118 ± 22 mL, P = 0.18, 63.5 ± 13.5 mL/m 2 vs. 63.0 ± 17.4 mL/m 2 , P = 0.83). Left–right shunting decreased from 40% ± 15% to 9% ± 15% ( P &lt; 0.001). Conclusion Cardiac MRI can reveal detailed information on acute changes in shunt fraction and ventricular dimensions after ASD closure. ASD closure by percutaneous transcatheter device implantation results within 24 hours in a significant reduction of shunt fraction, RA and RV sizes, and RV function, whereas LA and LV dimensions remain unchanged. J. Magn. Reson. Imaging 2007;25:1136–1140. © 2007 Wiley‐Liss, Inc.
A new approach for distinguishing cathepsin E and D activity in antigen‐processing organelles
2007-05-22

Cathepsin E (CatE) and D (CatD) are the major aspartic proteinases in the endolysosomal pathway. They have similar specificity and therefore it is difficult to distinguish between them, as known substrates are not exclusively specific for one or the other. In this paper we present a substrate‐based assay, which is highly relevant for immunological investigations because it detects both CatE and CatD in antigen‐processing organelles. Therefore it could be used to study the involvement of these proteinases in protein degradation and the processing of invariant chain. An assay combining a new monospecific CatE antibody and the substrate, MOCAc‐Gly‐Lys‐Pro‐Ile‐Leu‐Phe‐Phe‐Arg‐Leu‐Lys(Dnp)‐ d ‐Arg‐NH 2 [where MOCAc is (7‐methoxycoumarin‐4‐yl)acetyl and Dnp is dinitrophenyl], is presented. This substrate is digested by both proteinases and therefore can be used to detect total aspartic proteinase activity in biological samples. After depletion of CatE by immunoprecipitation, the remaining activity is due to CatD, and the decrease in activity can be assigned to CatE. The activity of CatE and CatD in cytosolic, endosomal and lysosomal fractions of B cells, dendritic cells and human keratinocytes was determined. The data clearly indicate that CatE activity is mainly located in endosomal compartments, and that of CatD in lysosomal compartments. Hence this assay can also be used to characterize subcellular fractions using CatE as an endosomal marker, whereas CatD is a well‐known lysosomal marker. The highest total aspartic proteinase activity was detected in dendritic cells, and the lowest in B cells. The assay presented exhibits a lower detection limit than common antibody‐based methods without lacking the specificity.
Expression of the Water Channel Protein Aquaporin-9 in Malignant Brain Tumors
2007-05-23

Recently, many studies seen concerning the expression and distribution of aquaporins and K channels in the central nervous system, and their physiological and pathophysiologic roles in water and ion homeostasis. Whereas most data were collected on aquaporin-4 (AQP4) in astrocytes, only little attention was paid to AQP9 which is a water channel transporting glycerol, mannitol, and urea as well. This is the first study describing AQP9 in human brain and human brain tumors. For comparison, we also investigated the immunohistochemical distribution of AQP9 in the rat glioma RG2. Whereas in the normal rat brain AQP9 is only weakly expressed by astrocytes, the anti-AQP9 immunoreactivity was found to be increased at the tumor border, but not within the tumor. In contrast, in human glioblastoma, most glioma cells throughout the tumor revealed a strong anti-AQP9 immunoreactivity across the whole surface of the cell. In the discussion, the increase of the anti-AQP9 immunoreactivity in glioma cells is suggested to reflect an upregulation and to counteract the glioma-associated lactic acidosis by clearance of glycerol and lactate from the extracellular space. In addition, the increased level of AQP9 immunoreactivity could be involved in the energy metabolism of the glioma and/or surrounding neuronal cells.
Cognitive function in patients with late stage amyotrophic lateral sclerosis
2007-05-23

The results of this study indicate a superior performance on learning and memory tasks of patients whose disease had further progressed. This may have important implications for our view on cognitive function in relation to the course of the disease.
From Forked Tongue to Forked Tongue: Rushdie and Milton in the Postcolonial Conversation
2007-05-23

In The Satanic Verses , Salman Rushdie draws heavily on Milton's Paradise Lost. However, unlike other postcolonial writers and theorists such as David Dabydeen and Dipesh Chakrabarty, Rushdie does not primarily polemicize against Milton as an embodiment of Europe's alleged cultural supremacy. Instead, his scattered references and allusions to Paradise Lost — especially to the figures of Satan, Adam and Eve — encourage a rereading of Milton as an unexpected precursor of postcolonial subjectivities. While the article offers close readings of some particularly rich instances of rewritings of Paradise Lost in The Satanic Verses, it also discusses aspects of other Milton texts in order to delineate that writer's ambiguous position towards questions of Empire, the “civilizing mission” and the centrality of the modern European subject.
Inhibiting TGF-β signaling restores immune surveillance in the SMA-560 glioma model
2007-05-24

Transforming growth factor-beta (TGF-beta) is a proinvasive and immunosuppressive cytokine that plays a major role in the malignant phenotype of gliomas. One novel strategy of disabling TGF-beta activity in gliomas is to disrupt the signaling cascade at the level of the TGF-beta receptor I (TGF-betaRI) kinase, thus abrogating TGF-beta-mediated invasiveness and immune suppression. SX-007, an orally active, small-molecule TGF-betaRI kinase inhibitor, was evaluated for its therapeutic potential in cell culture and in an in vivo glioma model. The syngeneic, orthotopic glioma model SMA-560 was used to evaluate the efficacy of SX-007. Cells were implanted into the striatum of VM/Dk mice. Dosing began three days after implantation and continued until the end of the study. Efficacy was established by assessing survival benefit. SX-007 dosed at 20 mg/kg p.o. once daily (q.d.) modulated TGF-beta signaling in the tumor and improved the median survival. Strikingly, approximately 25% of the treated animals were disease-free at the end of the study. Increasing the dose to 40 mg/kg q.d. or 20 mg/kg twice daily did not further improve efficacy. The data suggest that SX-007 can exert a therapeutic effect by reducing TGF-beta-mediated invasion and reversing immune suppression. SX-007 modulates the TGF-beta signaling pathway and is associated with improved survival in this glioma model. Survival benefit is due to reduced tumor invasion and reversal of TGF-beta-mediated immune suppression, allowing for rejection of the tumor. Together, these results suggest that treatment with a TGF-betaRI inhibitor may be useful in the treatment of glioblastoma.
Targeted mast cell silencing protects against joint destruction and angiogenesis in experimental arthritis in mice
2007-05-25

Abstract Objective Induction of arthritis with autoantibodies against glucose‐6‐phosphate isomerase (GPI) is entirely independent of T cells and B cells but is strictly dependent on the presence of mast cells. Here, we used this disease model to analyze whether exclusive intraarticular mast cell reconstitution is sufficient for disease induction and whether targeted mast cell silencing can prevent neoangiogenesis and joint destruction, 2 hallmarks of rheumatoid arthritis. Methods Ankle swelling and clinical index scores were determined after injection of either K/BxN mouse–derived serum or control serum in wild‐type Kit + / Kit + mice, congenic mast cell–deficient Kit W / Kit W ‐ v mice, or mast cell–deficient Kit W / Kit W ‐ v mice reconstituted with mast cells, either by intraperitoneal or selective intraarticular injection. Angiogenesis was quantified in vivo by measuring activated αvβ3 integrin using 18 F–galacto‐RGD and positron emission tomography. In addition, staining of joint tissue with hematoxylin and eosin, Giemsa, β3, and α‐actin was performed. The effect of mast cell stabilization by treatment with cromolyn or salbutamol was investigated in C57BL/6 or BALB/c mice. Results Comparing wild‐type mice, mast cell–deficient Kit W / Kit W ‐ v mice, and mast cell–reconstituted Kit W / Kit W ‐ v mice, we first showed that intraarticular and intraperitoneal mast cell engraftment fully restores susceptibility to antibody‐induced arthritis, angiogenesis, and αvβ3 integrin activation. Importantly, selective mast cell silencing with either salbutamol or cromolyn prevented αvβ3 integrin activation, angiogenesis, and joint destruction. Conclusion Mast cell engraftment fully restores susceptibility to αvβ3 integrin activation, angiogenesis, and joint destruction in GPI antibody–induced arthritis. Importantly, selective mast cell stabilization prevents αvβ3 integrin activation, angiogenesis, and joint destruction.
CdpNPT, an N‐Prenyltransferase from Aspergillus fumigatus: Overproduction, Purification and Biochemical Characterisation
2007-05-25

Abstract A putative prenyltransferase gene, cdpNPT , was identified in the genome sequence of Aspergillus fumigatus by a homology search by using known prenyltransferases and sequence analysis. CdpNPT consists of 440 amino acids and has a molecular mass of about 50 kDa. The coding sequence of cdpNPT was cloned in pQE60 and overexpressed in E. coli . The soluble His 6 ‐fusion CdpNPT was purified to near homogeneity and characterised biochemically. The enzyme showed broad substrate specificity towards aromatic substrates and was found to catalyse the prenylation of tryptophan‐containing cyclic dipeptides at N1 of the indole moieties in the presence of dimethylallyl diphosphate (DMAPP); geranyl diphosphate was not accepted as prenyl donor. The structures of the enzymatic products were elucidated by NMR and MS analysis. The K m value for DMAPP was determined to be 650 μ M . Due to substrate inhibition, K m values could not be obtained for the aromatic substrates. CdpNPT does not need divalent metal ions for its enzymatic reaction, although Ca 2+ enhances the reaction velocity by up to the threefold. CdpNPT is the first N‐prenyltransferase that has been purified and characterised in a homogenous form after heterologous overproduction. Interestingly, it shows significant sequence similarity to other indole prenyltransferases that catalyse the formation of CC bonds.
Somatostatin Receptor Subtype-2-Deficient Mice with Diet-Induced Obesity Have Hyperglycemia, Nonfasting Hyperglucagonemia, and Decreased Hepatic Glycogen Deposition
2007-05-25

Hypersecretion of glucagon contributes to abnormally increased hepatic glucose output in type 2 diabetes. Somatostatin (SST) inhibits murine glucagon secretion from isolated pancreatic islets via somatostatin receptor subtype-2 (sst2). Here, we characterize the role of sst2 in controlling glucose homeostasis in mice with diet-induced obesity. Sst2-deficient (sst2−/−) and control mice were fed high-fat diet for 14 wk, and the parameters of glucose homeostasis were monitored. Hepatic glycogen and lipid contents were quantified enzymatically and visualized histomorphologically. Enzymes regulating glycogen and lipid synthesis and breakdown were measured by real-time PCR and/or Western blot. Gluconeogenesis and glycogenolysis were determined from isolated primary hepatocytes and glucagon or insulin secretion from isolated pancreatic islets. Nonfasting glucose, glucagon, and fasting nonesterified fatty acids of sst2−/− mice were increased. Inhibition of glucagon secretion from sst2-deficient pancreatic islets by glucose or somatostatin was impaired. Insulin less potently reduced blood glucose concentration in sst2-deficient mice as compared with wild-type mice. Sst2-deficient mice had decreased nonfasting hepatic glycogen and lipid content. The activity/expression of enzymes controlling hepatic glycogen synthesis of sst2−/− mice was decreased, whereas enzymes facilitating glycogenolysis and lipolysis were increased. Somatostatin and an sst2-selective agonist decreased glucagon-induced glycogenolysis, without influencing de novo glucose production using cultured primary hepatocytes. This study demonstrates that ablation of sst2 leads to hyperglucagonemia. Increased glucagon concentration is associated with impaired glucose control in sst2−/− mice, resulting from decreased hepatic glucose storage, increased glycogen breakdown, and reduced lipid accumulation. Sst2 may constitute a therapeutic target to lower hyperglucagonemia in type 2 diabetes.
Ontogenetic Morphology and Allometry of the Cranium in the Common European Mole (Talpa europaea)
2007-05-25

Abstract The common European mole (Talpa europaea) has been the focus of many studies because of its fossorial lifestyle and related sensory and postcranial specializations. However, because of extensive fusion and pneumatization of the adult skull, many aspects of the cranial morphology of T. europaea are poorly understood. Here we present the 1st detailed study of cranial development in T. europaea, using an ontogenetic series of cleared and stained prenatal specimens to examine bone homologies, sequence of ossification, and prenatal allometry. The enigmatic lacrimal, jugal, and mastoid bones are all identified in prenatal specimens. The jugal and lacrimal bones fuse with the maxilla during prenatal growth, explaining previous difficulties with their identification in adults. T. europaea is anomalous among placental mammals in delaying the ossification of the alisphenoid and the orbitosphenoid until after birth. Analyses of allometry for 16 measures of individual bones show marked differences when postnatal specimens are included or excluded. Coefficients of allometry based on prenatal specimens are nearly twice those of analyses including subadult specimens. Comparisons with other taxa are limited by the lack of similar prenatal data, but the pattern exhibited by T. europaea differs significantly from those observed in studies of postnatal allometry in other mammals. These results may reflect differences among taxa or between prenatal and postnatal stages.
Standards and standardization in mastocytosis: Consensus Statements on Diagnostics, Treatment Recommendations and Response Criteria
2007-05-26

Abstract Although a classification for mastocytosis and diagnostic criteria are available, there remains a need to define standards for the application of diagnostic tests, clinical evaluations, and treatment responses. To address these demands, leading experts discussed current issues and standards in mastocytosis in a Working Conference. The present article provides the resulting outcome with consensus statements, which focus on the appropriate application of clinical and laboratory tests, patient selection for interventional therapy, and the selection of appropriate drugs. In addition, treatment response criteria for the various clinical conditions, disease‐specific symptoms, and specific pathologies are provided. Resulting recommendations and algorithms should greatly facilitate the management of patients with mastocytosis in clinical practice, selection of patients for therapies, and the conduct of clinical trials.
Total Synthesis of Cruentaren A
2007-05-27

A triple bypass: The triple bond in the macrolactone ring of 2 served as a lock to prevent the unwanted translactonization to the δ-lactone during the formation of the side chain of the macrolide cruentaren A (1). Subsequent cleavage of the methyl ether and the silicon protecting groups (PG) followed by a Lindlar reduction of the two triple bonds completed the synthesis (see scheme). Supporting information for this article is available on the WWW under http://www.wiley-vch.de/contents/jc_2002/2007/z701423_s.pdf or from the author. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.