gebhart/patrepeval huggingface dataset:
Sentence simplification for spoken language understanding (2011)

In this paper, we present a sentence simplification method and demonstrate its use to improve intent determination and slot filling tasks in spoken language understanding (SLU) systems. This research is motivated by the observation that, while current statistical SLU models usually perform accurately for simple, well-formed sentences, error rates increase for more complex, longer, more natural or spontaneous utterances. Furthermore, users familiar with web search usually formulate their information requests as a keyword search query, suggesting that frameworks which can handle both forms of inputs is required. We propose a dependency parsing-based sentence simplification approach that extracts a set of keywords from natural language sentences and uses those in addition to entire utterances for completing SLU tasks. We evaluated this approach using the well studied ATIS corpus with manual and automatic transcriptions and observed significant error reductions for both intent determination (30% relative) and slot filling (15% relative) tasks over the state-of the-art performances.
Whole-exome sequencing uncovers frequent GNAS mutations in intraductal papillary mucinous neoplasms of the pancreas (2011)

Intraductal papillary mucinous neoplasm (IPMN) is a common pancreatic cystic neoplasm that is often invasive and metastatic, resulting in a poor prognosis. Few molecular alterations unique to IPMN are known. We performed whole-exome sequencing for a primary IPMN tissue, which uncovered somatic mutations in KCNF1, DYNC1H1, PGCP, STAB1, PTPRM, PRPF8, RNASE3, SPHKAP, MLXIPL, VPS13C, PRCC, GNAS, KRAS, RBM10, RNF43, DOCK2, and CENPF. We further analyzed GNAS mutations in archival cases of 118 IPMNs and 32 pancreatic ductal adenocarcinomas (PDAs), which revealed that 48 (40.7%) of the 118 IPMNs but none of the 32 PDAs harbored GNAS mutations. G-protein alpha-subunit encoded by GNAS and its downstream targets, phosphorylated substrates of protein kinase A, were evidently expressed in IPMN; the latter was associated with neoplastic grade. These results indicate that GNAS mutations are common and specific for IPMN, and activation of G-protein signaling appears to play a pivotal role in IPMN.
Looking back (1979)

Abstract The following contribution from Dr. Holmes, founding editor of JCU , is the first of a series of short articles that will be published on the history of ultrasound technique. It is the firm belief of the present editor that a thorough appreciation of our roots is essential for understanding where we are going. How fortunate we are to have many of the real pioneers with us to relate their experiences.
AC-3: Flexible Perceptual Coding for Audio Transmission and Storage (1994)

Dolby AC-3 is a flexible audio data compression technology capable of encoding a range of audio channel formats into a low rate bit stream. Channel formats range from monophonic to 5.1 channels, and may include a number of associated audio services. Based on a transform filter bank and psychoacoustics, AC-3 includes the novel features of transmission of a variable frequency resolution spectral envelope and hybrid backward/forward adaptive bit allocation.
Parallel algorithms for data compression (1985)

Parallel algorithms for data compression by textual substitution that are suitable for VLSI implementation are studied. Both “static” and “dynamic” dictionary schemes are considered.
Control input shaping for coordinate measuring machines (2005)

Structural vibrations in coordinate measuring machines deteriorate measurement quality at high operating speeds. In this paper, a control strategy is presented that appropriately shapes inputs to a CMM motion controller in order to avoid exciting unwanted vibrations. This control strategy utilizes a traditional bang-bang trajectory and new filtering technique called the feedforward filter. The control input construction takes place in the discrete time domain and can be accomplished with considerably less computational effort than currently accepted methods. Experimental results show that utilizing a FF filtered trajectory results in approximately a 50% reduction in peak-to-peak magnitude of structural vibrations as compared to unshaped bang-bang trajectories.
Basic fibroblast growth factor protects endothelial cells against radiation-induced programmed cell death in vitro and in vivo. (1994)

Apoptosis (programmed cell death) serves as a common mechanism of interphase cell death after radiation exposure in thymic, lymphoid, and hematopoietic cells but has infrequently been documented in other adult mammalian cell types. The present study demonstrates that apoptotic interphase cell death occurs in endothelial cells after exposure to clinically relevant radiation doses and that basic fibroblast growth factor (bFGF) protects endothelial cells against this mode of the lethal effects of radiation. Radiation exposure produced heterologous double-stranded DNA breaks in endothelial cells, but the cells exhibited a similar competence for repair of this damage in the presence or absence of bFGF. However, subsequent to the completion of this repair process, a second process of DNA fragmentation became apparent, which was detected only in the absence of bFGF and was associated with a DNA ladder of oligonucleosomal fragments characteristic of apoptosis. The apoptotic DNA degradation occurred mainly in G0-G1 phase cells and was inhibited by bFGF stimulation. C3H/HeJ mice exposed to lethal doses of whole lung irradiation exhibited similar apoptotic changes in the endothelial cell lining of the pulmonary microvasculature within 6-8 h after radiation exposure. bFGF given i.v. immediately before and after irradiation inhibited the development of apoptosis in these cells and protected mice against the development of lethal radiation pneumonitis. These findings suggest that interphase apoptosis may represent a biologically relevant mechanism of radiation-induced cell kill in nonlymphoid mammalian cells both in vitro and in vivo and that natural protection mechanisms against this effect may be associated with the level of radiation resistance in normal and malignant tissues in vivo.
High temperature stability of Al2O3 dielectrics on Si: Interfacial metal diffusion and mobility degradation (2002)

We have examined the stability of Al2O3/Si heterostructures and show that significant Al diffusion occurs into the silicon for temperatures of 1000 °C and more. This may be caused by dissociation of small quantities of Al2O3 and subsequent dissolution of the Al into the silicon. Such diffusion may be reduced, though not eliminated via an interfacial silicon oxynitride diffusion barrier. Using long channel metal gate Al2O3/Si n field effect transistor data, we show that anneals at 1000 °C result in a degradation of the electron mobility by a factor of 2.
Hybridization properties of immobilized nucleic acids (1987)

The 5'-end attachment of oligonucleotides to dextran supports facilitates the study of the hybridization properties of an immobilized oligonucleotide system. The hybridization properties which were studied include: hybridization capacity and kinetics, hybridization-complex stability, and reagents influencing hybridization efficiency. Results of these experiments reveal that the hybridization efficiencies of support-bound oligonucleotides were 75-80% and 40-50% for single-stranded oligonucleotide targets and long double-stranded targets, respectively. These hybridization efficiencies are dependent upon prehybridizing the support-bound oligonucleotides with dextran sulfate. In addition, comparisons of the relative hybridization efficiencies of the support-bound oligonucleotide and nitrocellulose-based systems have been made which indicate a retention of 13-28% of target sequences on the filters and a detection efficiency of 8-20%.
Parathyroid Hormone-Induced Calcium Release from Intracellular Stores in a Human Kidney Cell Line in the Absence of Stimulation of Cyclic Adenosine 3',5'-Monophosphate Production (1997)

PTH-induced mobilization of cytosolic Ca2+ in a human kidney cell line (HEK/W) occurring in the absence of cAMP stimulation was characterized and compared with that obtained in the same cells stably transfected by the PTH/PTH-related peptide (PTHrp) receptor (HEK/T). In both cell lines, N-terminal fragments of PTH and PTHrp induced a concentration-dependent biphasic stimulation in[ Ca2+]i: a transient peak followed by a slow linear increase. These increases in [Ca2+]i were inhibited by the PTH antagonist[ Nle8,18,Tyr34]bPTH(3–34). The transient peaks were due to calcium release from intracellular stores, as they resisted quenching of calcium in the extracellular buffer and were abolished by prior emptying of intracellular stores. These peaks differed, however, both in latency period and in magnitude, in the two cell lines. The phospholipase C inhibitor U73122 inhibited the PTH-induced increase in [Ca2+]i in HEK/T cells, but not in HEK/W. Similarly, PTH-induced inositol phosphate (InsPs) production was detected in HEK/T but not in HEK/W cells. PTH-induced calcium release in HEK/W cells was inhibited by the simultaneous presence of ryanodine and U73122. Low level PTH/PTHrp receptor messenger RNA expression was demonstrated by ribonuclease protection in HEK/W cells, although no specific binding of[ 125I]PTHrP(1–34) could be detected. Amplification products for the PTH/PTHrp receptor 1, but no other isoforms, were detected by RT-PCR in HEK/W cells. As expected, HEK/T cells responded to PTH by a 500-fold stimulation in cAMP production and expressed large numbers of PTH/PTHrp receptors, as shown by [125I]PTHrp binding. These results demonstrate that the signal transduction pathways activated by PTH in HEK/W and HEK/T cells are different. Because the major difference in these cell lines is the number of PTH/PTHrp receptors expressed, these results suggest that the transduction of signals by the PTH/PTHrp receptor is controlled by receptor number in such a way that PTH stimulates an increase in intracellular calcium in the absence of stimulation of InsPs and cAMP production in cells expressing low levels of PTH/PTHrp receptor, but stimulates calcium release through an InsPs pathway and induces cAMP production in cells expressing large numbers of PTH/PTHrp receptors. The control of receptor number may be one of the mechanisms through which PTH effects are regulated.
A comparison of fibrin, agarose and gellan gum hydrogels as carriers of stem cells and growth factor delivery microspheres for cartilage regeneration (2013)

The limited intrinsic repair capacity of articular cartilage has led to the investigation of different treatment options to promote its regeneration. The delivery of hydrogels containing stem or progenitor cells and growth factor releasing microspheres represents an attractive approach to cartilage repair. In this study, the influence of the encapsulating hydrogel on the ability of progenitor cells coupled with TGF-β3 releasing microspheres to form cartilaginous tissue was investigated. Fibrin, agarose and gellan gum hydrogels containing TGF-β3 loaded gelatin microspheres and progenitor cells derived from the infrapatellar fat-pad of the knee were cultured for 21 days in a chemically defined media. In the presence of TGF-β3 releasing microspheres, gellan gum hydrogels were observed to facilitate greater cell proliferation than fibrin or agarose hydrogels. Histological and biochemical analysis of the hydrogels indicated that fibrin was the least chondro-inductive of the three hydrogels, while agarose and gellan gum appeared to support more robust cartilage formation as demonstrated by greater sGAG accumulation within these constructs. Gellan gum hydrogels also stained more intensely for collagen type II and collagen type I, suggesting that although total collagen synthesis was higher in these constructs, that the phenotype may be more fibrocartilaginous in nature than normal hyaline cartilage. This study demonstrates how the encapsulating hydrogel can have a significant impact on the ability of stem cells to form cartilage when incorporated into a growth factor delivery system.
Direct visualization of hemolymph flow in the heart of a grasshopper (Schistocerca americana) (2009)

Synchrotron x-ray phase contrast imaging is the only generally applicable technique that has the necessary spatial, temporal resolutions and sensitivity to directly visualize heart dynamics and flow patterns inside opaque animals. This technique has the potential to illuminate many long-standing questions regarding small animal circulation, encompassing topics such as retrograde heart flow in some insects and the development of flow in embryonic vertebrates.
Biofilms, infectious agents, and dental unit waterlines: a review (1998)

Aquatic biofilms, which are widespread not only in nature but also in medical and dental devices, can be the source of serious nosocomial infections. In these hardy microbial communities, pathogens like nontuberculous mycobacteria, Pseudomonas aeruginosa, Legionella pneumophila, and other bacteria not only survive but proliferate and lie in wait for susceptible hosts. Not only are these organisms intrinsically resistant to high temperatures and biocides, but the biofilms they inhabit enhance their resistance. This should be of concern to infection control practitioners. The bacterial colonization of dental unit waterlines can be used as a model to investigate the problem of waterborne biofilms in health care settings.Key words: dental unit waterlines, biofilm, nosocomial pathogens, drinking water.
The Role of NK Cells in Pig-to-Human Xenotransplantation (2017)

Recruitment of human NK cells to porcine tissues has been demonstrated in pig organs perfused ex vivo with human blood in the early 1990s. Subsequently, the molecular mechanisms leading to adhesion and cytotoxicity in human NK cell-porcine endothelial cell (pEC) interactions have been elucidated <i>in vitro</i> to identify targets for therapeutic interventions. Specific molecular strategies to overcome human anti-pig NK cell responses include (1) blocking of the molecular events leading to recruitment (chemotaxis, adhesion, and transmigration), (2) expression of human MHC class I molecules on pECs that inhibit NK cells, and (3) elimination or blocking of pig ligands for activating human NK receptors. The potential of cell-based strategies including tolerogenic dendritic cells (DC) and regulatory T cells (Treg) and the latest progress using transgenic pigs genetically modified to reduce xenogeneic NK cell responses are discussed. Finally, we present the status of phenotypic and functional characterization of nonhuman primate (NHP) NK cells, essential for studying their role in xenograft rejection using preclinical pig-to-NHP models, and summarize key advances and important perspectives for future research.
Further characterization of the cellular plasminogen binding site: evidence that plasminogen 2 and lipoprotein a compete for the same site (1989)

Specific cell surface receptors for plasminogen (Pg) are expressed by a wide variety of cell types and serve to promote fibrinolysis and local Pg proteolysis. Pg types 1 and 2, separated by chromatography on concanavalin A-Sepharose, were utilized to determine their binding to the monocytoid U937 cell line. Both forms bind in a dose-dependent manner. However, Pg 2 binds to the cellular receptor considerably better than Pg 1 and at equilibrium demonstrates approximately 10-fold greater binding. Lipoprotein a [Lp(a)], which possesses a subunit showing considerable homology to Pg, competes with Pg 2 for the Pg receptor in U937 cells. Moreover, Pg 1 is not able to displace Pg 2 from the receptor. These studies suggest that high levels of Lp(a) may alter the profibrinolytic activity at the cell surface and increase the risks of atherosclerosis and thrombosis. This hypothesis is in accord with the 2-5-fold increased risk of atherosclerosis in patients having high levels of Lp(a).
Evidence that accumulation of ceramides and cholesterol esters mediates oxidative stress–induced death of motor neurons in amyotrophic lateral sclerosis (2002)

Amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motor neurons in the spinal cord resulting in progressive paralysis and death. The pathogenic mechanism of ALS is unknown but may involve increased oxidative stress, overactivation of glutamate receptors, and apoptosis. We report abnormalities in sphingolipid and cholesterol metabolism in the spinal cords of ALS patients and in a transgenic mouse model (Cu/ZnSOD mutant mice), which manifest increased levels of sphingomyelin, ceramides, and cholesterol esters; in the Cu/ZnSOD mutant mice, these abnormalities precede the clinical phenotype. In ALS patients and Cu/Zn-SOD mutant mice, increased oxidative stress occurs in association with the lipid alterations, and exposure of cultured motor neurons to oxidative stress increases the accumulation of sphingomyelin, ceramides, and cholesterol esters. Pharmacological inhibition of sphingolipid synthesis prevents accumulation of ceramides, sphingomyelin, and cholesterol esters and protects motor neurons against death induced by oxidative and excitotoxic insults. These findings suggest a pivotal role for altered sphingolipid metabolism in the pathogenesis of ALS.
Emergence of oligodendrocytes from human neural spheres (1997)

To study the development of human oligodendrocyte precursors (OP), we expanded human embryonic brain-derived neural precursors into spheres with basic fibroblast growth factor (FGF2). Over 90% of the cells in the expanded spheres were precursors coexpressing nestin and the polysialylated (PSA) form of NCAM. The remaining cells were mostly astrocytes and neuronal cells located at the periphery of the floating spheres. When spheres were allowed to adhere on fibronectin-coated substrate in the absence of FGF2, neural precursors migrated in the outgrowth and often formed chains of cells expressing high levels of PSA-NCAM. Many migrating cells also expressed beta-3 tubulin while only scattered elongated cells radiating from the spheres were GFAP+ astrocytes. Spindle-shaped cells not associated with the chains were labeled for the PDGF-alpha receptor and often coexpressed MAP2 neuronal isoforms. Neuronal cells in the outgrowth rapidly established a rich neuritic network where OP expressing O4 and DM20/proteolipid antigens appeared. T3 treatment of neural spheres increased the rate of OP formation and the complexity of their shape. Thus, the generation of human oligodendrocytes from neural precursors is tightly correlated with growth of neuronal processes and enhanced by hormonal signals. J. Neurosci. Res. 50:146–156, 1997. © 1997 Wiley-Liss, Inc.
Iris Recognition: The Path Forward (2010)

Iris recognition systems have made tremendous inroads over the past decade, but work remains to improve their accuracy in environments characterized by unfavorable lighting, large stand-off distances, and moving subjects.
Positive Allosteric Modulators of Type 5 Metabotropic Glutamate Receptors (mGluR5) and Their Therapeutic Potential for the Treatment of CNS Disorders (2011)

Studies utilizing selective pharmacological antagonists or targeted gene deletion have demonstrated that type 5 metabotropic glutamate receptors (mGluR5) are critical mediators and potential therapeutic targets for the treatment of numerous disorders of the central nervous system (CNS), including depression, anxiety, drug addiction, chronic pain, Fragile X syndrome, Parkinson's disease, and gastroesophageal reflux disease. However, in recent years, the development of positive allosteric modulators (PAMs) of the mGluR5 receptor have revealed that allosteric activation of this receptor may also be of potential therapeutic benefit for the treatment of other CNS disorders, including schizophrenia, cognitive deficits associated with chronic drug use, and deficits in extinction learning. Here we summarize the discovery and characterization of various mGluR5 PAMs, with an emphasis on those that are systemically active. We will also review animal studies showing that these molecules have potential efficacy as novel antipsychotic agents. Finally, we will summarize findings that suggest that mGluR5 PAMs have pro-cognitive effects such as the ability to enhance synaptic plasticity, improve performance in various learning and memory tasks, including extinction of drug-seeking behavior, and reverse cognitive deficits produced by chronic drug use.
Identification of a binding site for blood coagulation factor IXa on the light chain of human factor VIII. (1994)

The interaction between human factor IXa and factor VIII or its constituent units was investigated. Equilibrium binding studies were performed employing factor VIII light chain that was immobilized on a monoclonal antibody. Factor VIII light chain was observed to bind factor IXa with high affinity (Kd = 14.8 +/- 3.2 nM) and approximately 1:1 stoichiometry. Optimal interaction required NaCl concentrations below 0.2 M and the presence of Ca2+ ions. Factor VIII light chain in solution effectively inhibited binding of factor IXa to the immobilized light chain (Ki = 10.9 +/- 1.9 nM). The isolated factor VIII light chain and the factor VIII heterodimer were equally effective in factor IXa binding, demonstrating that this interaction did not require the factor VIII heavy chain. Factor Xa and activated Protein C were found to be inefficient (Ki > or = 1.2 microM) in competing with factor IXa, indicating that the high affinity for factor VIII light chain was unique for factor IXa. The factor IXa-factor VIII light chain interaction was inhibited by von Willebrand factor, but this effect was abolished by cleavage of the factor VIII light chain by thrombin. An antibody that inhibits von Willebrand factor-factor VIII complex formation did not compete for factor IXa binding. In contrast, association of factor IXa with the factor VIII light chain was inhibited by an antibody directed against the factor VIII region Gln1778-Asp1840. We propose that this sequence provides a factor IXa binding site and that its exposure requires dissociation of the factor VIII-von Willebrand factor complex.
Peripheral and Central Mechanisms of Inflammatory Pain, with Emphasis on MAP Kinases (2004)

Tissue injury is associated with inflammation and produces inflammatory pain. In animal models, inflammatory pain is normally produced by injection of irritative chemicals into the hindpaw or joint of animal. Inflammatory pain manifests as an expression of neuronal plasticity, which consists of peripheral sensitization (increased sensitivity of primary sensory neurons in the peripheral nervous system, PNS) and central sensitization (increased sensitivity of spinal dorsal horn and other neurons in the central nervous system, CNS). Activation of several protein kinases causes both forms of sensitization via posttranslational, translational, and transcriptional regulation. In particular, mitogen-activated protein kinase (MAPK), such as ERK and p38, is activated by inflammatory mediators in primary sensory and secondary order dorsal horn neurons and participates in the generation and maintenance of inflammatory pain. Development of specific MAPK inhibitors will open a new avenue to the pharmacological intervention of inflammatory pain.